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Environmental conditions in food and medical fields enable the bacteria to attach and grow on surfaces leading to resistant bacterial biofilm formation. Indeed, the first step in biofilm formation is the bacterial irreversible adhesion. Controlling and inhibiting this adhesion is a passive approach to fight against biofilm development. This strategy is an interesting path in the inhibition of biofilm formation since it targets the first step of biofilm development. Those pathogenic structures are responsible for several foodborne diseases and nosocomial infections. Therefore, to face this public health threat, researchers employed cold plasma technologies in coating development. In this review, the different factors influencing the bacterial adhesion to a substrate are outlined. The goal is to present the passive coating strategies aiming to prevent biofilm formation via cold plasma treatments, highlighting antiadhesive elaborated surfaces. General aspects of surface treatment, including physico-chemical modification and application of cold plasma technologies, were also presented. KEY POINTS: • Factors surrounding pathogenic bacteria influence biofilm development. • Controlling bacterial adhesion prevents biofilm formation. • Materials can be coated via cold plasma to inhibit bacterial adhesion., (© 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

The persistence of Salmonella enterica on abiotic surfaces in hospitals and the agri-food industries leads to several infections worldwide. In this context, this work aimed to study the adhesion of S. Enteritidis on plasma-modified stainless steel to prevent biofilm-associated-infections. Surface modification was achieved by the elaboration of organosilicon coatings from the monomer 1,1,3,3-tetramethyldisiloxane, mixed with oxygen, using a flowing nitrogen microwave post-discharge plasma polymerization technique. The effect of cold plasma parameters on the properties of the coatings, the coated surface topography and S. Enteritidis cell adhesion was studied. The results showed that the surface topography influenced the bacterial adhesion rate. Indeed, rough surfaces did not repel S. Enteritidis since the number of attached cells on these coatings was between 30 ± 4 to 65 ± 4 bacteria per microscopic field. Otherwise, smoother surfaces demonstrated an anti-adhesive character since the number of attached cells was almost nil on these coatings.

Objective: Pre-eclampsia (PE) is a serious disease of pregnancy and one of the major causes of morbidity and mortality for both the mother and baby. This systematic review aims to detect the role of high-sensitivity C-reactive protein (CRP) in the detection of PE., Methods: Thirty-four articles published between 2001 and 2019 were included in this review. The articles were extracted from OVID Medline and Embase. The study designs of these articles are randomized controlled, cohort, case-control, and cross-sectional studies evaluating CRP as a marker to predict or early diagnose PE. The quality assessment of these articles is made by the modified Quality Assessment of Diagnostic Accuracy Studies 2 tool. Meta-analysis was not done because of clinical and statistical heterogeneity., Results: A positive association between CRP levels and the development of PE was confirmed in 18 studies. This positive effect was addressed in patients with normal BMI (<25 kg/m2) in 3 studies and in overweight patients in 2 studies. One study addressed this positive association in patients with a BMI ranging between 28 and 31 kg/m2. Three studies determined a cutoff level of CRP above which a significant risk of PE development should be suspected. These levels ranged between 7 and 15 mg/L., Conclusion: CRP is a promising cost-effective biomarker that may be used in the prediction of PE. A CRP level higher than 15 mg/L may suggest initiation of low-dose aspirin in low-risk pregnancies., (© 2021 S. Karger AG, Basel.)

We have previously established a model to study the in vivo human IgE response using humanized SCID mice. Allergic SCID mice were obtained following intraperitoneal injection with mononuclear cells from Dermatophagoides pteronyssinus (Dpt)-sensitive patients, and sensitization by Dpt allergen intraperitoneal injection (immunization) or Dpt aerosol (inhalation). Human serum IgE was measured in allergic SCID mice after administration of human recombinant IFN-gamma or the lipopeptide LP 52-71 (derived from peptide p52-71 from Der p 1, Dpt major allergen, coupled to a lipophilic moiety), during the immunization or the inhalation phase. IFN-gamma inhibited human IgE production when given at the time of immunization, but not during inhalation. This effect was long-lasting as Dpt aerosol, given one month after immunization and IFN-gamma administration, failed to increase IgE levels. Unlike Dpt or p52-71, LP 52-71 failed to induce human IgE production at day 14 and 21 after its injection, but did inhibit the development of the IgE response after a secondary Dpt-challenge. Moreover, LP 52-71 administration 14 days after Dpt inhalation decreased IgE levels, in contrast to peptide 52-71, which increased IgE levels. Thus, taken together these results indicate that the development of the human IgE response in allergic SCID mice can be modulated by modified allergen and a Th1 cytokine.

Background: T lymphocytes are important components of the bronchial inflammatory cell infiltrate in asthma. Because lymphocytes activated in the respiratory tract recirculate to remote glandular and mucosal sites, we previously studied the histologic features of minor salivary glands (MSGs) in bronchial asthma and found an airway-like inflammation with T-lymphocyte infiltration, the presence of mast cells that were often degranulated, and basement membrane thickening but no eosinophil infiltration., Objective: We sought to investigate the cellular infiltration and cytokine profile in MSGs from untreated asthmatic subjects, steroid-treated asthmatic subjects, and control subjects and to compare these values with those found in bronchial biopsy specimens., Methods: The cellular infiltration was studied by using immunohistochemistry. Cytokine messenger (m)RNA expression for IL-4, IL-5, and IFN-gamma was determined by using in situ hybridization and cytokine immunoreactivity with immunohistochemistry., Results: A significant increase in CD4 and IL-4 mRNA(+) cells was observed in MSGs from asthmatic patients (both untreated and steroid-treated subjects) when compared with control subjects, which correlated with the clinical severity of asthma (FEV(1) and Aas score). In contrast to the bronchi, no IL-5 mRNA expression was observed in MSGs, and no difference was observed for MSG IFN-gamma mRNA between the groups. At the level of MSG protein expression, the 3 cytokines were seen, with a significant increase in IL-4 protein expression in steroid-treated asthmatic subjects compared with untreated asthmatic subjects and control subjects, but there were no differences between the groups in IL-5 and IFN-gamma protein expression., Conclusion: The cytokine mRNA expression pattern observed in the MSGs of asthmatic subjects was different from that found in the bronchi, suggesting a different local immune regulation.

The mechanism by which specific immunotherapy exerts its beneficial effect remains unclear. Chemokines are implicated in inflammatory and allergic diseases, in particular via their ability to induce histamine release from basophils, a potential early target of rush venom immunotherapy (RVIT), In this study, the authors evaluated ex vivo regulated upon activation normal T-cell expressed and secreted (RANTES), interleukin 8 (IL-8) and monocyte chemoattractant protein 1 (MCP-1) production and mRNA expression by mononuclear cells (MNC) from nine patients undergoing a 3.5-h ultra rush treatment, before treatment at Day 0 (D0), at the end of the 3.5-h of the rush at Day 4h (D4h), at Day 15 (D15) and Day 45 (D45) after treatment. Increased RANTES release and mRNA expression were observed in 24-h culture of peripheral blood MNC collected at D4h. This was followed by a decrease in the production of RANTES, IL-8 and MCP-1, 45 days after initiation of RVIT. The same pattern was observed after in vitro venom stimulation of MNC. At the mRNA level, similar profiles were observed except for IL-8 mRNA which inversely increased during RVIT. These results suggest that RVIT is associated with a general decrease in chemokines which may explain, in part, the clinical efficacy of specific immunotherapy., (Copyright 1998 Academic Press.)

We have developed an animal model to study human delayed-type hypersensitivity reactions. Previous studies in humans have shown after tuberculin injection the presence of a mononuclear cell infiltration, with almost no eosinophils, associated with a preferential Th-1-type cytokine profile. Human skin graft obtained from tuberculin-reactive donors was grafted onto the back of severe combined immunodeficient mice. After healing, mice were reconstituted intraperitoneally with peripheral mononuclear cells. Tuberculin and diluent were injected intradermally, and skin biopsies were performed 72 hours later. Skin grafts were divided into two parts, one for immunohistochemistry and one for in situ hybridization studies. Immunohistochemistry was performed on cryostat sections using the alkaline phosphatase anti-alkaline phosphatase technique. In the tuberculin-injected sites as compared with the diluent-injected sites, there were significant increases in the number of CD45+ pan leukocytes and CD4+, CD8+, CD45RO+ T cells but not in CD68+ monocytes/macrophages and EG2 or MBP+ eosinophils. The activation markers CD25 and HLA-DR were up-regulated in the tuberculin-injected sites. In situ hybridization was performed using 35S-labeled riboprobes for interleukin (IL)-2, interferon (IFN)-gamma, IL-4, and IL-5. After tuberculin injection, a preferential Th-1-type cytokine profile was observed with significant increases in the numbers of IL-2 and IFN-gamma mRNA-expressing cells. These results are similar to those reported after tuberculin-induced delayed-type hypersensitivity in humans, suggesting that this model might be useful to study cutaneous inflammatory reaction.