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The nexus between eosinophils and microbes is attracting increasing attention. We previously showed that airway administration of sterile microbial products contained in dust collected from traditional dairy farms virtually abrogated bronchoalveolar lavage (BAL) eosinophilia and other cardinal asthma phenotypes in allergen-sensitized specific pathogen-free (SPF) mice. Interestingly, comparable inhibition of allergen-induced BAL eosinophilia and promotion of airway barrier integrity were found upon administration of a sterile, pharmacological-grade bacterial lysate, OM-85, to the airway compartment of allergen-sensitized SPF mice. Here, we asked whether intrinsic properties of airway-delivered microbial products were sufficient to inhibit allergic lung inflammation or whether these effects were mediated by reprogramming of the host microbiota. We compared germ-free (GF) mice and offspring of GF mice associated with healthy mouse gut microbiota and maintained under SPF conditions for multiple generations (Ex-GF mice). These mice were treated intranasally with OM-85 and evaluated in the ovalbumin and Alternaria models of allergic asthma focusing primarily on BAL eosinophilia. Levels of allergen-induced BAL eosinophilia were comparable in GF and conventionalized Ex-GF mice. Airway administration of the OM-85 bacterial lysate was sufficient to inhibit allergen-induced lung eosinophilia in both Ex-GF and GF mice, suggesting that host microbiota are not required for the protective effects of bacterial products in these models and local airway exposure to microbial products is an effective source of protection. OM-85-dependent inhibition of BAL eosinophilia in GF mice was accompanied by suppression of lung type 2 cytokines and eosinophil-attracting chemokines, suggesting that OM-85 may work at least by decreasing eosinophil lung recruitment., Competing Interests: Conflict of interest statement. D.V. and V.P. are inventors in PCT/EP2019/074562 (“Method of Treating and/or Preventing Asthma, Asthma Exacerbations, Allergic Asthma and/or Associated Conditions with Microbiota Related to Respiratory Disorders”). The rest of the authors have no relevant conflicts of interest., (© The Author(s) 2024. Published by Oxford University Press on behalf of Society for Leukocyte Biology.)

Rationale: Eosinophilic pulmonary disease (EPD) is a general term for a large group of diseases with complex etiology. Ulcerative colitis is an inflammatory bowel disease (IBD). Patients with IBD may have pulmonary involvement. We herein present a case of ulcerative colitis complicated with EPD., Patient Concerns: A 34-year-old woman with ulcerative colitis presented with dry cough. She had peripheral eosinophilia and apical ground glass opacities on CT (computed tomography) of her chest. Antibiotic treatment was ineffective., Diagnoses: Lung biopsy revealed eosinophil infiltration in the alveolar space and interstitial space, so EPD was considered., Interventions: After oral administration of prednisone, the lung shadow on CT disappeared when the cough symptoms resolved. However, the symptoms recurred after drug withdrawal, and the lung shadow reappeared on imaging. The cough symptoms and lung shadow disappeared after oral prednisone was given again. Prednisone was slowly discontinued after 6 months of treatment., Outcomes: The patient stopped prednisone for half a year. No recurrence or abnormal CT findings were detected during the half-year follow-up., Lessons: The clinical manifestations of EPD are atypical, laboratory and imaging findings are not specific, and it is difficult to make a definite diagnosis before lung biopsy. The diagnosis depends on pathological examination. Glucocorticoid treatment is effective, but some patients may relapse after drug withdrawal. Active follow-up after glucocorticoid treatment is very important for identifying disease recurrence. Patients with IBD are relatively prone to developing EPD. The etiology of EPD is complex. In clinical practice, we need to make a diagnosis and differential diagnosis to clarify its etiology., Competing Interests: The authors have no funding and conflicts of interest to disclose., (Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.)

Pulmonary and extrapulmonary complications after coronavirus disease 2019 (COVID-19) have been major public health concerns during the COVID-19 pandemic. Although post-COVID-19 pulmonary manifestations cover a wide spectrum, eosinophilic pneumonia (EP) has rarely been reported. To date, only four cases of EP potentially triggered by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection have been reported, all of which required systemic corticosteroid therapy. We herein report the first case of post-COVID-19 EP resolution without systemic corticosteroid therapy. We also review the literature regarding EP associated with SARS-CoV-2 infection and vaccination.

Background: Acute eosinophilic pneumonia (AEP) is well-known as one of the primary eosinophilic pulmonary diseases of unknown etiology. It's defined as a febrile illness along with acute onset respiratory failure that is commonly misdiagnosed at the initial presentation as infectious pneumonia. Despite the fact that AEP sometimes classified as idiopathic as no exact cause can be identified in most cases, it has been suggested recently to be linked with electronic cigarette or vaping products and associated with electronic cigarette or vaping associated lung injury (EVALI). Therefore, history of recent tobacco smoking or vaping exposure along with peripheral eosinophilia are crucial clinical findings suggestive of AEP., Case Presentation: A previously healthy 17-year-old female presented to the Emergency Room with one day history of progressively worsening shortness of breath accompanied by left sided pleuritic chest pain and fever. She wasn't taking any medications, denied traditional cigarette smoking, exposure to pulmonary irritants, recent travel and had no history of close contact with sick patient. She recently started vaping 20 days prior to the presentation. Initially, she was admitted with a presumptive diagnosis of atypical pneumonia but was found to have AEP due to a recent vaping exposure., Conclusion: Vaping is a well-known health hazard that has become a growing trend among adolescents and have been promoted as a safe and effective alternative to traditional cigarettes. The etiology of AEP remains unclear, but many studies suggest a possible link with recent tobacco smoking or vaping. A key challenge for this clinical entity is to reach the diagnosis after excluding all other pulmonary eosinophilia causes, and it has an excellent prognosis if diagnosed early and treated appropriately., (© 2023. BioMed Central Ltd., part of Springer Nature.)

The role of eosinophil and migratory dendritic cell (migDC) subsets during tropical pulmonary eosinophilia (TPE), a potentially fatal complication of lymphatic filariasis, has not been explored. We show that the onset of TPE is characterized by the accumulation of ROS and anaphylatoxins and a rapid influx of morphologically distinct Siglec-F int resident eosinophils (rEos) and Siglec-F hi inflammatory eosinophils (iEos) in the lungs, BAL fluid, and blood of TPE mice. While rEos display regulatory behavior, iEos are highly inflammatory cells, as evident in upregulated expression of activation markers CD69 and CD101, anaphylatoxin receptor C5AR1, alarmins s100a8 and s100a9, components of NADPH oxidase, and copious secretion of TNF-α, IFN-γ, IL-6, IL-1β, IL-4, IL-10, IL-12, and TGF-β. Importantly, iEos exhibited heightened ROS generation, higher phagocytic and increased antigen presentation capacity, elevated Ca 2+ influx, and increased F-actin polymerization but downregulated negative regulators of the immune response, i.e., Cd300a, Anaxa1, Runx3, Lilrb3, and Serpinb1a, underlining their essential role in promoting lung damage during TPE. Interestingly, TPE mice also showed significant expansion of CD24 + CD11b + migDCs, which showed upregulated expression of maturation and costimulatory markers CD40, CD80, CD83, CD86, and MHCII, increased antigen presentation capacity, and higher migratory potential as evidenced by increased expression of cytokine receptors CCR4, CCR5, CXCR4, and CXCR5. CD24 + CD11b + migDCs also upregulated the expression of immunoregulators PD-L1 and PD-L2 and secreted proinflammatory cytokines, suggesting their significant involvement during TPE. Taken together, we document important morphological, immunophenotypic, and functional characteristics of eosinophil and migDC subsets in the lungs of TPE mice and suggest that they contribute to worsening lung histopathological conditions during TPE.

Rationale: The relationship between rheumatoid arthritis (RA) and eosinophilic inflammation is unclear. According to recent studies, it has been suggested that T helper 2 cell responses play a role in the inhibition of RA. It is unclear how the immunological response after coronavirus disease-2019 (COVID-19) vaccination affects T cell immune reactions., Patient Concerns and Diagnoses: Here, we report the case of an 88-year-old woman diagnosed with RA and chronic eosinophilic pneumonia (CEP). She was diagnosed with CEP about 20 years ago, and, through steroid treatment, she improved and had no relapse for 16 years. At the time of diagnosis of CEP, the rheumatoid factor (RF) was increased; however, there were no joint symptoms. After receiving the COVID-19 vaccine, joint and respiratory symptoms gradually worsened. Laboratory examinations showed increased RF, anti-cyclin citrullinated peptide antibody, and peripheral absolute eosinophil count. Musculoskeletal ultrasonography showed synovitis., Intervention and Outcome: Methylprednisolone pulse therapy improved respiratory and joint symptoms immediately; RA and CEP stabilized with no relapses., Lessons: Eosinophilic and rheumatoid reactions following COVID-19 vaccination were an-reported adverse events. Eosinophilic inflammation might be reflected on an anti-inflammatory reaction in initial phase of RA., (Copyright © 2022 the Author(s). Published by Wolters Kluwer Health, Inc.)

Group 2 innate lymphoid cells (ILC2s) are tissue resident in the lung and activated by inhaled allergens via epithelial-derived alarmins including IL-33. Activated ILC2s proliferate, produce IL-5 and IL-13, and induce eosinophilic inflammation. Here, we report that intranasal IL-33 or the protease allergen papain administration resulted in increased numbers of ILC2s not only in the lung but also in peripheral blood and liver. Analyses of IL-33 treated parabiosis mice showed that the increase in lung ILC2s was due to proliferation of lung resident ILC2s, whereas the increase in liver ILC2s was due to the migration of activated lung ILC2s. Lung-derived ILC2s induced eosinophilic hepatitis and expression of fibrosis-related genes. Intranasal IL-33 pre-treatment also attenuated concanavalin A-induced acute hepatitis and cirrhosis. These results suggest that activated lung resident ILC2s emigrate from the lung, circulate, settle in the liver and promote type 2 inflammation and attenuate type 1 inflammation., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Mathä, Romera-Hernández, Steer, Yin, Orangi, Shim, Chang, Rossi and Takei.)

Studying the proteomes of tissue-derived extracellular vesicles (EVs) can lead to the identification of biomarkers of disease and can provide a better understanding of cell-to-cell communication in both healthy and diseased tissue. The aim of this study was to apply our previously established tissue-derived EV isolation protocol to mouse lungs in order to determine the changes in the proteomes of lung tissue-derived EVs during allergen-induced eosinophilic airway inflammation. A mouse model for allergic airway inflammation was used by sensitizing the mice intraperitoneal with ovalbumin (OVA), and one week after the final sensitization, the mice were challenged intranasal with OVA or PBS. The animals were sacrificed 24 h after the final challenge, and their lungs were removed and sliced into smaller pieces that were incubated in culture media with DNase I and Collagenase D for 30 min at 37 °C. Vesicles were isolated from the medium by ultracentrifugation and bottom-loaded iodixanol density cushions, and the proteomes were determined using quantitative mass spectrometry. More EVs were present in the lungs of the OVA-challenged mice compared to the PBS-challenged control mice. In total, 4510 proteins were quantified in all samples. Among them, over 1000 proteins were significantly altered (fold change >2), with 614 proteins being increased and 425 proteins being decreased in the EVs from OVA-challenged mice compared to EVs from PBS-challenged animals. The associated cellular components and biological processes were analyzed for the altered EV proteins, and the proteins enriched during allergen-induced airway inflammation were mainly associated with gene ontology (GO) terms related to immune responses. In conclusion, EVs can be isolated from mouse lung tissue, and the EVs' proteomes undergo changes in response to allergen-induced airway inflammation. This suggests that the composition of lung-derived EVs is altered in diseases associated with inflammation of the lung, which may have implications in type-2 driven eosinophilic asthma pathogenesis.

Idiopathic hypereosinophilic syndrome (IHES) is a rare myeloproliferative disease characterised by multisystem dysfunction and persistent, extreme eosinophilia of unknown cause. Here we present a 42-year-old patient complaining of moderate to severe chest pain and shortness of breath, and typical ischaemic electrocardiography changes were recorded. He was initially suspected of having acute coronary syndrome, however the coronary angiogram excluded coronary abnormalities. Bone marrow biopsy, left ventriculography, transthoracic echocardiography and cardiac magnetic resonance examinations confirmed the diagnosis of IHES and IHES-mediated cardiac involvement. The patient's illness was alleviated during the first hospitalisation, whereas it had rapidly worsened one month after discharge. In addition, simultaneous pulmonary and skin-infiltrating lesions occurred during the second hospitalisation. The patient's condition improved markedly with combined glucocorticoid, hydroxyurea and warfarin therapy, as well as treatment for heart failure. In this report the diagnostic modalities and treatment strategies for IHES are discussed and reviewed.

Background: Eosinophils develop from CD34 + progenitor cells in the bone marrow under the influence of interleukin (IL)-5. Several cell types produce IL-5, including type 2 innate lymphoid cells (ILC2s). The alarmin cytokine IL-33 is known to activate ILC2s in mucosal tissues, but little is known about IL-33-responsive ILC2s in the bone marrow in allergen-induced airway inflammation. Methods: Wild type (WT) and Rag1 deficient ( Rag1 -/- ) mice, which lack mature T and B cells, received intranasal doses of papain to induce acute allergic inflammation. In some experiments, mice were pre-treated with anti-IL-5 prior to the papain challenge. Furthermore, recombinant IL-33 was administered to WT mice, Rag1 -/- mice, lymphocyte deficient mice ( Rag2 -/- Il2rg -/- ) and to ex vivo whole bone marrow cultures. Bone marrow eosinophils and ILC2s were analyzed by flow cytometry. Eosinophil count was assessed by differential cell count and secreted IL-5 from bone marrow cells by ELISA. Results: Intranasal administration of papain or IL-33 increased the number of mature eosinophils in the bone marrow despite the absence of adaptive immune cells in Rag1 -/- mice. In parallel, an increased number of eosinophils was observed in the airways together with elevated levels of Eotaxin-2/CCL24. Bone marrow ILC2s were increased after papain or IL-33 administration, whereas ILC2s was found to be increased at baseline in Rag1 -/- mice compared to WT mice. An upregulation of the IL-33 receptor (ST2) expression on bone marrow ILC2s was observed after papain challenge in both Rag1 -/- and WT mice which correlated to increased number of bone marrow eosinophilia. Furthermore, an increased number of ST2 + mature eosinophils in the bone marrow was observed after papain challenge, which was further dependent on IL-5. In addition, bone marrow-derived ILC2s from both mouse strains produced large amounts of IL-5 ex vivo after IL-33 stimulation of whole bone marrow cultures. In contrast, IL-33-induced bone marrow and airway eosinophilia were abolished in the absence of ILC2s in Rag2 -/- Il2rg -/- mice and no production of IL-5 was detected in IL-33-stimulated bone marrow cultures. Conclusion: These findings establish bone marrow ILC2s and the IL-33/ST2 axis as promising targets for modulation of uncontrolled IL-5-dependent eosinophilic diseases including asthma., (Copyright © 2020 Boberg, Johansson, Malmhäll, Calvén, Weidner and Rådinger.)

Although elevated blood or sputum eosinophils are present in many patients with COPD, uncertainties remain regarding the anatomical distribution pattern of lung-infiltrating eosinophils. Basophils have remained virtually unexplored in COPD. This study mapped tissue-infiltrating eosinophils, basophils and eosinophil-promoting immune mechanisms in COPD-affected lungs.Surgical lung tissue and biopsies from major anatomical compartments were obtained from COPD patients with severity grades Global Initiative for Chronic Obstructive Lung Disease stages I-IV; never-smokers/smokers served as controls. Automated immunohistochemistry and in situ hybridisation identified immune cells, the type 2 immunity marker GATA3 and eotaxins (CCL11, CCL24).Eosinophils and basophils were present in all anatomical compartments of COPD-affected lungs and increased significantly in very severe COPD. The eosinophilia was strikingly patchy, and focal eosinophil-rich microenvironments were spatially linked with GATA3 + cells, including type 2 helper T-cell lymphocytes and type 2 innate lymphoid cells. A similarly localised and interleukin-33/ST2-dependent eosinophilia was demonstrated in influenza-infected mice. Both mice and patients displayed spatially confined eotaxin signatures with CCL11 + fibroblasts and CCL24 + macrophages.In addition to identifying tissue basophilia as a novel feature of advanced COPD, the identification of spatially confined eosinophil-rich type 2 microenvironments represents a novel type of heterogeneity in the immunopathology of COPD that is likely to have implications for personalised treatment., Competing Interests: Conflict of interest: P. Jogdand has nothing to disclose. Conflict of interest: P. Siddhuraj has nothing to disclose. Conflict of interest: M. Mori has nothing to disclose. Conflict of interest: C. Sanden has nothing to disclose. Conflict of interest: J. Jönsson has nothing to disclose. Conflict of interest: A.F. Walls has nothing to disclose. Conflict of interest: J. Kearley is an employee of AstraZeneca (formerly MedImmune LLC) and has stock options in AstraZeneca. Conflict of interest: A.A. Humbles was an employee of AstraZeneca (formerly MedImmune LLC) at the time these analyses were conducted. Conflict of interest: R. Kolbeck was an employee of AstraZeneca (formerly MedImmune LLC) at the time these analyses were conducted. Conflict of interest: L. Bjermer has nothing to disclose. Conflict of interest: P. Newbold is an employee of AstraZeneca (formerly MedImmune LLC) and has stock options in AstraZeneca. Conflict of interest: J.S. Erjefält is founder (and stock owner) of Medetect AB, who received funding from AstraZeneca for conducting parts of the present study., (Copyright ©ERS 2020.)

Idiopathic acute eosinophilic pneumonia is a rare and potentially life-threatening condition that is defined by bilateral pulmonary infiltrates and fever in the presence of pulmonary eosinophilia. It often presents acutely in previously healthy individuals and can be difficult to distinguish from infectious pneumonia. Although the exact etiology of idiopathic acute eosinophilic pneumonia remains unknown, an acute hypersensitivity reaction to an inhaled antigen is suggested, which is further supported by recent public health risks of vaping (electronic cigarette) use and the development of lung disease. In this case, a patient with a year-long history of vaping in conjunction with tetrahydrocannabinol cartridge use who was diagnosed with idiopathic acute eosinophilic pneumonia with associated bilateral hilar lymphadenopathy is described., Competing Interests: POTENTIAL CONFLICT OF INTEREST: The authors have indicated they have no potential conflicts of interest to disclose., (Copyright © 2020 by the American Academy of Pediatrics.)

A 27-year-old, previously physically healthy man presented to an emergency department with an acute onset of thoracic pain, dyspnea, non-productive cough and fever. Hours before the onset of symptoms, the patient has smoked tobacco using a waterpipe (spearmint taste, not commercially available in Germany). Due to a progressive respiratory failure the patient required invasive mechanical ventilation. The computertomography scan of the chest showed bilateral diffuse, infiltrative changes. The diagnosis of hookah smoking associated Acute Eosinophilic Pneumonia (AEP) was based on the patient's history, the eosinophilic count in broncho-alveolar lavage and the computertomographic findings. After treatment with corticosteroids, the patient could be extubated after 9 days. The outpatient follow-up revealed a normal lung function testing and X-ray of the chest without any physical sequelae. CONCLUSION:  In cases of acute onset of thoracic pain, dyspnea, non-productive cough and fever, acute eosinophilic pneumonia should be considered for differential diagnosis in association with shisha smoking. Severe respiratory lung failure can be successfully treated with corticosteroid therapy and ventilation resulting in full recovery., Competing Interests: Die Autorinnen/Autoren geben an, dass kein Interessenkonflikt besteht., (© Georg Thieme Verlag KG Stuttgart · New York.)

Pulmonary manifestations of inflammatory bowel disease are increasingly recognized in patients with ulcerative colitis and Crohn's disease. Most commonly, incidental abnormalities are noted on chest imaging or pulmonary function tests. Although clinically significant pulmonary disease is less common, it can carry significant morbidity for patients. We review the presenting symptoms, workup, and management for several of the more common forms of inflammatory bowel disease-related pulmonary disease. Increased awareness of the spectrum of extraintestinal inflammatory bowel disease will help providers more readily recognize this phenomenon in their own patients and more comprehensively address the protean sequelae of inflammatory bowel disease., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Background: Eosinophilic lung diseases represent a heterogeneous group of disorders with prominent infiltrate of eosinophils in lung interstitium and alveolar spaces. Peripheral blood eosinophilia is often present. Infections, drugs, allergens, toxic agents have to be evaluated as possible causes of eosinophilic lung infiltrates. The category of myeloid/lymphoid neoplasms with eosinophilia and rearrangement of PDGFRA, PDGFRB, FGFR1 and PCM1-JAK2 represents an uncommon cause of eosinophilic lung infiltrate., Case Presentation: We report the case of a 70-year old man complaining of dry cough and dyspnea. Ground glass-opacities were seen on imaging studies and peripheral blood eosinophilia was present. A thorough step-wise patient's evaluation led to identify the clonal nature of eosinophilia and the diagnosis of myeloid/lymphoid neoplasm with eosinophilia and rearrangement of PDGFRA was made., Conclusions: Correlation with clinical history, laboratory tests and imaging studies is essential to achieve the correct diagnosis when facing with eosinophilic lung infiltrates. A prolonged eosinophilia can cause life-threatening organ damage. Identification of PDGFRA rearrangement, as in the present case, is particularly critical given the sensitivity and excellent response to imatinib, which has completely changed the natural history of this neoplasm.

Calprotectin is a heterodimer of the proteins S100A8 and S100A9, and it is an abundant innate immune protein associated with inflammation. In humans, calprotectin transcription and protein abundance are associated with asthma and disease severity. However, mechanistic studies in experimental asthma models have been inconclusive, identifying both protective and pathogenic effects of calprotectin. To clarify the role of calprotectin in asthma, calprotectin-deficient S100A9 -/- and wild-type (WT) C57BL/6 mice were compared in a murine model of allergic airway inflammation. Mice were intranasally challenged with extracts of the clinically relevant allergen, Alternaria alternata (Alt Ext), or PBS every third day over 9 days. On Day 10, BAL fluid and lung tissue homogenates were harvested and allergic airway inflammation was assessed. Alt Ext challenge induced release of S100A8/S100A9 to the alveolar space and increased protein expression in the alveolar epithelium of WT mice. Compared with WT mice, S100A9 -/- mice displayed significantly enhanced allergic airway inflammation, including production of IL-13, CCL11, CCL24, serum IgE, eosinophil recruitment, and airway resistance and elastance. In response to Alt Ext, S100A9 -/- mice accumulated significantly more IL-13 + IL-5 + CD4 + T-helper type 2 cells. S100A9 -/- mice also accumulated a significantly lower proportion of CD4 + T regulatory (Treg) cells in the lung that had significantly lower expression of CD25. Calprotectin enhanced WT Treg cell suppressive activity in vitro . Therefore, this study identifies a role for the innate immune protein, S100A9, in protection from CD4 + T-helper type 2 cell hyperinflammation in response to Alt Ext. This protection is mediated, at least in part, by CD4 + Treg cell function.

Eosinophilic pneumonia (EP) is a rare disorder, comprising several heterogeneous diseases. Two major types of EP are acute eosinophilic pneumonia (AEP) and chronic eosinophilic pneumonia (CEP), both of which are characterized by marked accumulation of eosinophils in lung tissues and/or BAL fluid. AEP and CEP share some similarities in terms of pathophysiology, radiological findings, and treatment response to corticosteroids. However, they distinctly differ in etiology, clinical manifestations, and the nature of disease course. Especially, although AEP and CEP respond well to corticosteroids, relapse frequently occurs in patients with CEP, but rarely in those with AEP. Although CEP occasionally persists and becomes corticosteroid dependent, most patients with AEP completely recover. This article reviews previous studies and discusses the etiology, clinical manifestations, and treatment of AEP and CEP., (Copyright © 2019 Japanese Society of Allergology. Production and hosting by Elsevier B.V. All rights reserved.)

Ascariasis is a soil-sourced, second most common parasitic infection worldwide. Because of its wandering nature, it migrates from the intestine to other organs of the body like the lungs and biliary system. This results in complications such as biliary colic, acute cholecystitis, pyogenic cholangitis, liver abscesses, pancreatitis and loeffler's pneumonia. We report a unique case of an 8-year-old boy who presented with upper gastrointestinal bleed and chest infection. He was diagnosed as haemobilia and loeffler's pneumonia caused by ascaris lumbricoides., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2019. No commercial re-use. See rights and permissions. Published by BMJ.)

The spectrum of eosinophilic lung diseases comprises a diverse group of pulmonary disorders associated with tissue or peripheral eosinophilia. [Acute eosinophilic pneumonia (AEP)] is an uncommon eosinophilic lung disease that can be idiopathic, but identifiable causes include medications, inhalational exposures and infections. Most cases in the literature are associated with first-time cigarette smoking or resuming smoking. Herein, we present a case of AEP in an elderly man triggered by exposure to secondhand tobacco smoke, in whom a transbronchial biopsy was diagnostic. The patient recovered fully with glucocorticoid therapy without recurrence after avoiding further secondhand smoke.

Introduction: The impact of immune checkpoint blockade on immunity in cancer patients is not completely elucidated due to the complexity of the immune network. Recent studies have revealed a significant role of programed cell death-ligand 2 (PD-L2) in negatively controlling the production of CD4+ T helper type 2 (Th2) cytokines and airway hypersensitiveness, suggesting hypo-responsive Th2 cells via the PD-1/PD-L2 inhibitory pathway in lung could be reawaken by PD-1 blockade therapy., Methods: We describe the first report of acute eosinophilic pneumonia (AEP), which is known as Th2-associated pulmonary disease, triggered by nivolumab, an anti-PD-1 antibody, in an advanced non-small cell lung cancer patient. Based on the current case report and literature, the present study proposes a potential mechanism of the onset of AEP as an immune-related adverse event (irAE)., Results: A 62-year-old man was diagnosed with lung adenocarcinoma and nivolumab was selected as the third-line regimen. After three cycles of nivolumab treatment, chest computed tomography revealed pulmonary infiltrates in both lungs. The patient was diagnosed with AEP based on the diagnostic criteria for AEP. Nivolumab was suspended and the patient was started on oral prednisolone. His symptoms and radiological findings had rapidly improved., Conclusions: Given the increasing frequency of the use of anti-PD-1 antibodies, clinicians should be aware of the risk of AEP as a potential irAE. This study may improve our understanding of the pathophysiology underlying Th2-associated irAEs and AEP., (© 2018 The Authors. Immunity, Inflammation and DiseasePublished by John Wiley & Sons Ltd. Published by John Wiley & Sons Ltd.)

Background: Eosinophilic pneumonia (EP) is characterized by massive pulmonary infiltration by eosinophils. Although serum periostin is a novel marker for eosinophil-dominant asthma, the upregulation of periostin in the airway of asthmatics is controversial. In this study, we examined whether periostin concentrations are elevated in the bronchoalveolar lavage fluid (BALF) of patients with EP., Methods: BAL was performed in healthy volunteers and in patients with acute eosinophilic pneumonia (AEP), chronic eosinophilic pneumonia (CEP), and sarcoidosis. The periostin concentrations in the BALF were measured., Results: The periostin concentration in the BALF increased significantly with pulmonary eosinophil ia and was higher in AEP and CEP patients than in healthy volunteers and sarcoidosis patients, even after adjusting the albumin concentration. In pulmonary eosinophilia, the periostin concentration correlated with the eosinophil and lymphocyte counts, the concentration of albumin, and the concentration of cytokines such as IL-5, IL-13, and transforming growth factor β1., Conclusions: Although some blood leakage may be involved in the elevation of periostin in the BALF of EP, periostin can be induced locally, at least in part. Therefore, periostin may play a role in the development of EP., (© 2019 S. Karger AG, Basel.)

Background: Most patients with acute eosinophilic pneumonia (AEP) show rapid improvement. However, some cases of AEP prove fatal. The aims of this study were to determine the clinical, radiographic, and pathologic characteristics of patients in whom AEP has a fatal outcome and to identify predictors of a poor prognosis., Methods: We retrospectively identified the medical records of all patients diagnosed with AEP at our institution in Japan from July 2005 to July 2013., Results: There were four deaths among 41 patients diagnosed to have AEP during the study period. All the patients who died were male; three cases were idiopathic and one was medication-related. The median bronchoalveolar lavage eosinophil differential count was 59%. An autopsy was performed on the patient with medication-related AEP who died and the pathologic finding was diffuse alveolar damage with eosinophilic infiltration. Diffuse ground-glass attenuation and traction bronchiectasis (TBE) were identified on high-resolution computed tomography in the four patients with fatal AEP. TBE was observed in six patients (five with idiopathic AEP, one with medication-related AEP), and 67% of these patients died. None of the patients with smoking-related AEP had TBE; all these patients had better responses to treatment and survived., Conclusions: We observed the characteristics of patients with fatal AEP who did not respond to treatment. TBE was observed in all fatal cases and may be associated with a poor prognosis., (Copyright © 2018 The Japanese Respiratory Society. Published by Elsevier B.V. All rights reserved.)

Marijuana use has risen dramatically over the past decade. Over this same time period, pediatric hospitals have seen an increase in presentation of adolescents with acute respiratory symptoms after recent marijuana inhalation. We report a case series of three adolescent males with significant findings of bilateral pulmonary nodules and ground glass opacities on chest imaging associated with recent marijuana inhalation. Lung biopsies in two of the three patients confirmed silica-induced pneumoconiosis. The third patient was diagnosed with acute hypersensitivity pneumonitis without lung biopsy. Improvement in clinical symptoms and lung function testing were noted in two of three patients after marijuana inhalation cessation. This case series highlights the variety of severe pulmonary presentations in adolescents following recent marijuana inhalation. Future studies are required to assess whether these presenting pulmonary complications are from direct marijuana exposure or indirect associations with marijuana inhalation injuries., (© 2018 Wiley Periodicals, Inc.)

Rationale: Extensive thrombosis in the portal venous system caused by hypereosinophilic syndrome (HES) is rare, and there is no consensus on anticoagulant and thrombolytic treatments for arteriovenous thrombosis caused by HES., Patient Concerns: The clinical data of a patient with extensive thrombosis in his portal venous system (superior mesenteric, splenic, hepatic, and portal veins), renal artery thrombosis, and mesenteric thrombosis caused by HES with secondary gastrointestinal bleeding and intestinal necrosis were retrospectively analyzed. Before admission, his eosinophil count increased to 7.47 × 10/L, and HES had been confirmed via bone marrow cytology. The patient experienced fever, cough, abdominal pain, massive hematemesis, and hematochezia that developed in succession. Abdominal computed tomography showed portal vein and superior mesenteric vein thromboses., Diagnosis: Hypereosinophilic syndrome; extensive thrombosis in the portal venous system; acute eosinophil-associated pneumonia; gastrointestinal bleeding; intestinal necrosis., Interventions: The patient was first treated with methylprednisolone, plasma exchange/hemofiltration, and single or combined use of unfractionated heparin and argatroban for anticoagulation. He was also administered alteplase and urokinase, successively, for thrombolytic treatment. Once the thromboses finally disappeared, the patient underwent surgery to excise a necrotic intestinal canal., Outcomes: The thromboses disappeared with these treatments, and the patient recovered after the necrotic intestinal canal was excised., Lessons: The clinical manifestations of HES are complex and varied, and this condition can cause severe and extensive arteriovenous thrombosis. Anticoagulation therapy and thrombolysis are necessary interventions, and appear to be safe and effective.

Eosinophilia (EOS) is an important component of airway inflammation and hyperresponsiveness in allergic reactions including those leading to asthma. Although cigarette smoking (CS) is a significant contributor to long-term adverse outcomes in these lung disorders, there are also the curious reports of its ability to produce acute suppression of inflammatory responses including EOS through poorly understood mechanisms. One possibility is that proinflammatory processes are suppressed by nicotine in CS acting through nicotinic receptor α7 (α7). Here we addressed the role of α7 in modulating EOS with two mouse models of an allergic response: house dust mites (HDM; Dermatophagoides sp.) and ovalbumin (OVA). The influence of α7 on EOS was experimentally resolved in wild-type mice or in mice in which a point mutation of the α7 receptor (α7 E260A:G ) selectively restricts normal signaling of cellular responses. RNA analysis of alveolar macrophages and the distal lung epithelium indicates that normal α7 function robustly impacts gene expression in the epithelium to HDM and OVA but to different degrees. Notable was allergen-specific α7 modulation of Ccl11 and Ccl24 (eotaxins) expression, which was enhanced in HDM but suppressed in OVA EOS. CS suppressed EOS induced by both OVA and HDM, as well as the inflammatory genes involved, regardless of α7 genotype. These results suggest that EOS in response to HDM or OVA is through signaling pathways that are modulated in a cell-specific manner by α7 and are distinct from CS suppression.

Rationale: Eosinophilic pleural effusion in elderly patients is most commonly due to malignancies and infections., Patient Concerns: In rare cases, pleural eosinophilia is associated with connective tissue disease., Diagnoses: Presence of Hargraves cells, also called lupus erythematosus (LE) cells (polynuclear cells that have engulfed denatured nuclear material), was a key point of American College of Rheumatology (ACR) classification criteria for systemic lupus erythematosus (SLE) until 1997. Now replaced by serology for autoantibodies, LE cells characterization remains useful in guiding the diagnostic strategy towards autoimmune diseases., Interventions: An 82-year-old woman complained about anorexia, weight loss, fatigue, and mild night fever. Clinical examination disclosed a left pleural effusion without parenchymal lesion on high contrast thoraco-abdomino-pelvic computed tomography scan. A thoracocentesis revealed an exudate with eosinophilia. Direct cytological examination showed LE cells. SLE was rapidly considered. Antinuclear antibodies were subsequently found in the serum and in the pleural effusion. Anti-nucleosome antibodies were also present without antiphospholipid antibodies. Her condition rapidly improved after initiation of prednisone and hydroxychloroquine., Outcomes: Six months later, the patient had no particular complain, clinical examination was strictly normal biological parameter were in normal range., Lessons: The assessment of an eosinophilic pleural effusion allowed to find LE cells, which rapidly suggested the diagnosis of SLE, and early initiation of appropriate treatment. LE cells are no longer a criterion for the diagnosis of SLE, but their presence in serosa is most helpful in guiding the diagnostic strategy, and specifically in atypical forms often seen in older patients.

Background: IL-37 is emerging as an anti-inflammatory cytokine, particularly in innate inflammation. However, the role of IL-37 in Th2-mediated allergic lung inflammation remains uncertain. We sought to determine the role and the underlying mechanisms of IL-37 in the development of house dust mites (HDM)-induced murine asthma model., Methods: We examined the effect of IL-37 administration during the sensitization or challenge phase on Th2-mediated allergic asthma induced by inhaled HDM. Cellular source of CCL11 and distribution of IL-37 receptors, IL-18Rα and IL-1R8, were determined in HDM-exposed lungs. Finally, we examined the effect of IL-37 on CCL11 production and STAT6 activation in different primary lung structural cell types upon IL-4/IL-13 stimulation., Results: IL-37 had no effect on HDM sensitization, but when administrated during the challenge phase, significantly attenuated pulmonary eosinophilia, CCL11 production, and airway hyper-reactivity (AHR). Interestingly, IL-37 treatment had no significant effects on lung infiltrating T cells and Th2 cytokine production. Intranasal co-administration of CCL11 reversed the inhibiting effect of IL-37 on HDM-induced pulmonary eosinophilia and AHR. Furthermore, we demonstrated that CCL11 was primarily expressed by fibroblasts and airway smooth muscle cells (AMSC), while IL-37 receptors by tracheobronchial epithelial cells (TEC). In vitro study showed that IL-37 inhibited IL-4/IL-13-induced STAT6 activation and CCL11 production by fibroblasts and AMSC, which was dependent on its direct action on TEC. Moreover, cell contact was required for the inhibitory effect of IL-37-treated TEC., Conclusions: IL-37 attenuates HDM-induced asthma, possibly by inhibiting IL-4/IL-13-induced CCL11 production by fibroblasts and AMSC via its direct act on TEC., (© 2018 EAACI and John Wiley and Sons A/S. Published by John Wiley and Sons Ltd.)

Over the past decade, smoking behaviors have changed in the US. Hookah or waterpipe smoking is increasing, especially among youth and young adults. Social media sites describe the "hookah high" or "buzz", which may be related to nicotine, carbon monoxide, or other inhalants in hookah smoke. Most important is the risk of carbon monoxide poisoning. Case reports include a high number of victims presenting with loss of consciousness from either syncope or seizures. Anaphylaxis and a very rare respiratory hypersensitivity reaction, acute eosinophilic pneumonia, have also been reported from hookah smoking in previously healthy young adults. This article provides background information on hookah smoking, describes hookah-induced acute injuries that could precipitate poison center calls, and offers suggestions for exposure characterization.

Understanding functions of Foxp3 + regulatory T cells (Tregs) during allergic airway inflammation remains incomplete. In this study, we report that, during cockroach Ag-induced allergic airway inflammation, Foxp3 + Tregs are rapidly mobilized into the inflamed lung tissues. However, the level of Treg accumulation in the lung was different depending on the type of inflammation. During eosinophilic airway inflammation, ∼30% of lung-infiltrating CD4 T cells express Foxp3, indicative of Tregs. On the contrary, only ∼10% of infiltrating CD4 T cells express Foxp3 during neutrophilic airway inflammation. Despite the different accumulation, the lung inflammation and inflammatory T cell responses were aggravated following Treg depletion, regardless of the type of inflammation, suggesting regulatory roles for Tregs. Interestingly, however, the extent to which inflammatory responses are aggravated by Treg depletion was significantly greater during eosinophilic airway inflammation. Indeed, lung-infiltrating Tregs exhibit phenotypic and functional features associated with potent suppression. Our results demonstrate that Tregs are essential regulators of inflammation, regardless of the type of inflammation, although the mechanisms used by Tregs to control inflammation may be shaped by environmental cues available to them., (Copyright © 2017 by The American Association of Immunologists, Inc.)

Purpose: Chronic graft versus host disease (cGvHD) is a common complication of hematopoietic stem cell transplantation (HSCT). Eosinophilic lung disease is a rare poorly understood complication in HSCT patients with cGvHD. These patients present similarly to those with Acute Eosinophilic Pneumonia (AEP). The purpose of this study is to better elucidate the presentation and potential treatment of this phenomenon., Methods: We reviewed over 170 bronchoscopies in post-HSCT patients with respiratory symptoms. Of these, four patients, whose course was complicated by cGvHD, presented with respiratory symptoms, diffuse ground-glass opacities (GGO) on chest computerized tomography (CT), bronchoalveolar lavage (BAL) eosinophilia, and no evidence of infection. The clinical course of these patients was reviewed., Results: Despite clinical presentation similar to AEP, not all patients had > 25% eosinophils on BAL, one criterion for AEP, however all improved with steroids. Steroid initiation was often delayed in favor of empiric antibiotics despite negative infectious workup. Several patients had recurrent episodes. Regarding possible associations, we examined but found no link between particular demographics, reason for HSCT, chemotherapy, immunosuppressants, or peripheral eosinophil count and pulmonary eosinophilia in these patients. GGO present on initial CT imaging became chronic in several of these patients., Conclusion: We propose that in post-HSCT patients with GvHD presenting with respiratory symptoms, GGO on CT, BAL eosinophilia of > 10%, and negative respiratory cultures, an autoimmune eosinophilic process may be occurring. Earlier recognition and initiation of corticosteroids in these patients may improve their outcomes as an autoimmune diagnosis was often delayed in favor of antibiotics.

Introduction: The relationship between bronchodilator responsiveness and eosinophilic airway inflammation has not been well documented in COPD. It has been investigated in this retrospective study. This issue has grown in importance due to increasing interest in the asthma-COPD overlap syndrome., Methods: 264 stable COPD patients with no past history of asthma were retrospectively analyzed. Correlation analyses between FEV 1 reversibility and sputum eosinophil levels were conducted. Sputum eosinophil levels were dichotomized using FEV 1 reversibility cut-off points (>0.4L and >15% vs. >0.2L and >12%) and compared. The effectiveness of FEV 1 reversibility to predict sputum eosinophilia (>3%) was analyzed with a logistic regression and a ROC analysis., Results: 82 (31.1%) patients with higher FEV 1 reversibility values (0.14 vs. 0.11L, P=.01) presented sputum eosinophilia. FEV 1 reversibility was weakly correlated with the sputum eosinophil level (r=0.162, P=.008). Patients with FEV 1 >0.4L and >15% increment had higher sputum eosinophil levels (6.11 vs. 1.02%, P=.049) whereas the level did not differ when dichotomized by FEV 1 increment >0.2L and >12%. Very positive FEV 1 reversibility (>0.4L and >15%) predicted sputum eosinophilia after adjustment forage, baseline FEV 1 and FVC (OR: 4.262, P=.029). In the ROC analysis, the AUC was 0.58 (P=.034), and FEV 1 increment>0.4L and >15% had a positive predictive value of 63.6% and an overall accuracy of 70.1%., Conclusions: FEV 1 reversibility was weakly correlated with sputum eosinophil levels in COPD. Positive FEV 1 reversibility (>0.4L and >15%) is moderately successful in predicting sputum eosinophilia (>3%)., (Copyright © 2017 SEPAR. Publicado por Elsevier España, S.L.U. All rights reserved.)

Cutaneous larva migrans is a frequent dermatologic problem among travelers in tropical areas, but its association with Löffler's syndrome is an extremely rare condition, particularly in children. Here, we describe a 6-year-old boy presenting cutaneous larva migrans associated with Löffler's syndrome.

Airway eosinophilia is a hallmark of allergic asthma, and understanding mechanisms that promote increases in lung eosinophil numbers is important for effective pharmacotherapeutic development. It has become evident that expansion of hematopoietic compartments in the bone marrow (BM) promotes differentiation and trafficking of mature eosinophils to the airways. Hematopoietic progenitor cells egress the BM and home to the lungs, where in situ differentiation within the tissue provides an ongoing source of proinflammatory cells. In addition, hematopoietic progenitor cells in the airways can respond to locally derived alarmins to produce a panoply of cytokines, thereby themselves acting as effector proinflammatory cells that potentiate type 2 responses in eosinophilic asthma. In this review, we provide evidence for these findings and discuss novel targets for modulating eosinophilopoietic processes, migration, and effector function of precursor cells., (Copyright © 2017 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Background: Acute eosinophilic pneumonia (AEP) is an uncommon disease, often indistinguishable from ARDS or community-acquired pneumonia at initial presentation. AEP can be idiopathic, but identifiable causes include medications and inhalational exposures, including cigarette smoke., Methods: Using a computer-assisted search, we retrospectively identified and reviewed the medical records of all patients diagnosed with AEP between January 1, 1998, and June 30, 2016, at our institution. Demographic and clinical data were extracted, including exposures (occupational, environmental, recreational, pharmacologic, and smoking), laboratory and radiologic findings, treatments, hospitalization (including ICU stay), and subsequent clinical course., Results: Among 36 consecutive patients with AEP, 11 were smoking-related cases, six were medication-related cases and 19 were idiopathic. Smoking-related AEP included six first-time smokers and five ex-smokers who had resumed smoking after a period of abstinence. Patients with smoking-related AEP were younger compared with both medication-related and idiopathic AEP cases (median age: 22 vs 47.5 vs 55 years, respectively; P = .004). Patients with smoking-related AEP were less likely to be associated with peripheral eosinophilia at presentation (36% vs 50% vs 58%; P = .52) but more likely to be hospitalized (100% vs 50% vs 63%; P = .039), including a longer ICU stay, compared with medication-related and idiopathic cases., Conclusions: AEP is associated with a good prognosis when recognized and treated promptly. Compared with medication-related and idiopathic AEP, smoking-related AEP was less likely to be associated with peripheral eosinophilia at presentation but was characterized by more severe disease manifestations., (Copyright © 2017 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

The lung develops an unique epithelial barrier system to protect host from continuous invasion of various harmful particles. Interleukin (IL-)33 released from epithelial cells in the lung drives the type 2 immune response by activating ST2- expressed immune cells in various allergic diseases. However, the involvement of memory-type ST2 + CD4 + T cells in such lung inflammation remains unclear. Here we demonstrated that intratracheal administration of IL-33 resulted in the substantial increase of numbers of tissue-resident memory-type ST2 + CD4 + T cells in the lung. Following enhanced production of IL-5 and IL-13, eosinophilic lung inflammation sequentially developed. IL-33-mediated eosinophilic lung inflammation was not fully developed in T cell-deficient Foxn1 nu mice and NSG mice. Dexamethasone treatment showed limited effects on both the cell number and function of memory-type ST2 + CD4 + T cells. Thus our study provides novel insight into the pathogenesis of eosinophilic lung disease, showing that memory-type ST2 + CD4 + T cells are involved in IL-33-induced eosinophilic inflammation and elicited steroid-resistance.

A man in his 20s with no medical history presented with 2 days of progressively worsening shortness of breath accompanied by subjective fevers, chills, body aches, decreased appetite, night sweats, and cough producing nonbloody sputum. He denied childhood lung diseases, allergies, or a family history of lung disease. He did not smoke cigarettes but had smoked hookah in Saudi Arabia before moving to the United States 1 month before presentation and had restarted 2 days before the start of symptoms. He denied travel outside of the northeastern United States. He did not take medications, use illicit drugs, or engage in high-risk behavior., (Copyright © 2016 American College of Chest Physicians. Published by Elsevier Inc. All rights reserved.)

Urban particulate matter (PM) is associated with an increase in asthma. PM2.5 (

Background: Inhaled corticosteroids are important in the management of chronic obstructive pulmonary disease (COPD), but can slightly increase the risk of pneumonia in patients with moderate-to-severe COPD. Patients with circulating eosinophil counts of 2% or more of blood leucocytes respond better to inhaled corticosteroids than do those with counts of less than 2% and it was therefore postulated that blood eosinophil count might also have an effect on the risk of pneumonia in patients with COPD. In this post-hoc meta-analysis, we investigate whether a 2% threshold can identify patients who differ in their risk of pneumonia, irrespective of inhaled corticosteroid treatment., Methods: From the GlaxoSmithKline trial registry, we selected randomised, double-blind, clinical trials of patients with COPD that had: inhaled corticosteroid arms (fluticasone propionate and salmeterol or fluticasone furoate and vilanterol); a control arm (not given inhaled fluticasone); and pre-randomisation measurements of blood eosinophil counts and were of at least 24 weeks in duration. With use of specified terms from the Medical Dictionary for Regulatory Activities we identified pneumonia adverse events in patient-level data. We calculated number of patients with pneumonia events, stratified by baseline blood eosinophil count (<2% vs ≥2% of blood leucocytes) and whether or not patients had received inhaled corticosteroids., Findings: We identified ten trials (conducted between 1998 and 2011), with eosinophil count data available for 10 861 patients with COPD. 4043 patients had baseline blood eosinophil counts of less than 2% and 6818 patients had baseline blood eosinophil counts of 2% or more. 149 (3·7%) patients with counts less than 2% had one or more pneumonia adverse events compared with 215 (3·2%) with counts of 2% or more (hazard ratio [HR] 1·31; 95% CI 1·06-1·62). In patients not treated with inhaled corticosteroids, 40 (3·8%) patients with less than 2% blood eosinophil counts had a pneumonia event versus 48 (2·4%) with 2% or more blood eosinophils (HR 1·53; 95% CI 1·01-2·31). In patients treated with inhaled corticosteroids, events occurred in 107 (4·5%) versus 164 (3·9%; HR 1·25; 95% CI 0·98-1·60), respectively., Interpretation: Using 2% baseline eosinophil count as a threshold, patients with COPD with lower blood eosinophil counts had more pneumonia events than did those with higher counts. The magnitude of this increased risk was small and should be further explored in large, prospective studies. These data should be considered when making treatment decisions, alongside existing evidence that patients with COPD and baseline blood eosinophil counts less than 2% have a poorer response to inhaled corticosteroids., Funding: GlaxoSmithKline., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

The diagnosis of eosinophilic pneumonia is rare and malignant etiology remains exceptional. Eosinophilic pneumonia etiology varies and is mainly dominated by allergic and drug causes. We report the case of a 61-year-old patient with B-cell non-Hodgkin lymphoma revealed by eosinophilic pneumonia. The diagnosis of eosinophilic pneumonia was confirmed by eosinophil count of 56% in bronchoalveolar lavage. Immunohistochemical examination of bone marrow biopsy revealed malignant Small B cells non-Hodgkin lymphoma., Competing Interests: Conflits d’intérêts Les auteurs ne déclarent aucun conflit d'intérêt.

We report the case of a young male patient with a solitary pulmonary echinococcus cyst. The diagnosis of Cystic Echinococcosis is based on clinical findings, imaging and serology. In the setting of lung cysts the diagnosis can be difficult, particularly as the sensitivity of the serologic tests is lower compared to liver cysts. Bronchoscopic ultrasound of the cystic lesion and respectively the analysis of the cyst aspirate can lead to the diagnosis. In the present case an eosinophilic pneumonia as the result of the puncture has to be discussed., (© Georg Thieme Verlag KG Stuttgart · New York.)