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Background: The most recent guideline on acute pulmonary embolism (PE) indicates possible long-term sequelae such as dyspnoea and chronic thromboembolic pulmonary hypertension after a PE event. However, effects on lung function or asthma risk have not been evaluated in the general population., Methods: We tested whether individuals with a venous thromboembolism (VTE) encompassing PE and deep vein thrombosis (DVT) have reduced lung function, or greater risks of dyspnoea and asthma using data from 102 792 adults from the Copenhagen General Population Study. Diagnoses of PE, DVT and asthma were collected from the national Danish Patient Registry. Factor V Leiden and prothrombin G20210A gene variants were determined using TaqMan assays., Results: Prevalences of PE, DVT and VTE were 2.2%, 3.6% and 5.2%, respectively. Individuals with VTE had forced expiratory volume in 1 s of 92% predicted compared with 96% pred in individuals without VTE (p<0.001). Individuals with VTE versus those without had adjusted OR (95% CI) for light, moderate and severe dyspnoea of 1.4 (1.2-1.6), 1.6 (1.4-1.8) and 1.7 (1.5-1.9), respectively. Individuals with VTE versus those without had an adjusted OR for asthma of 1.6 (95% CI 1.4-1.8). Factor V Leiden and prothrombin G20210A genotype also associated with increased risk of asthma (p for trend=0.002). Population-attributable fractions of severe dyspnoea and asthma due to VTE were 3.5% and 3.0%, respectively, in the population., Conclusion: Individuals with VTE have worse lung function and higher risks of severe dyspnoea and asthma, and may account for 3.5% and 3.0% of people with severe dyspnoea and asthma, respectively, in the general population., Competing Interests: Conflict of interest: None declared., (Copyright ©The authors 2023.)

Parental asthma or allergy have been linked to higher risk of asthma in a child; this occurs to a variable extent in different study populations. Moreover, it is debated whether maternal more so than paternal asthma history is a stronger predisposing factor: while in some countries/populations the maternal effect was clearly seen over paternal, in others the parental effects were equivalent, and in a few studies paternal effect dominated. Here we aimed to determine parental asthma and allergy effect in the Danish GEneral SUburban population Study (GESUS). This cross-sectional study has involved 21,362 adults aged 20+ years in the suburbs of Copenhagen. We used a combination of questionnaire approach, history of prescribed asthma medications and pulmonary function testing to determine odds ratios for maternal and paternal (and combined) asthma and allergy linked to asthma in the test subjects. We found that the input of maternal vs. paternal asthma effect was approximately equal (age and sex-adjusted OR 2.46, 95% CI: 2.15-2.81 for asthmatic mothers vs. 2.97, 2.58-3.42 for asthmatic fathers), except for the "ever asthma" age and sex-adjusted odds ratios where paternal allergy seems to have conferred a marginally greater effect (age and sex-adj. OR 1.96 for maternal allergy vs. 2.44 for paternal allergy, p = 0.03). Stratifying for gestational tobacco smoking did not affect the maternal results. We conclude that in the GESUS study parental asthma or allergy were strongly linked to higher asthma risk in offspring, without a prominent maternal or paternal effect., Competing Interests: Declaration of competing interest Please find attached our original research article titled “Risk of asthma in offspring of asthmatic fathers versus mothers: A population-based study of 21,000 individuals in Denmark”. The authors declare no conflict of interest., (Copyright © 2023 Elsevier Ltd. All rights reserved.)

Background: Increased elastase activity in α 1 -antitrypsin deficiency may affect elasticity of the arterial walls, and thereby blood pressure and susceptibility to cardiovascular disease. We hypothesized that severe α 1 -antitrypsin deficiency is associated with reduced blood pressure and susceptibility to cardiovascular disease., Methods: We genotyped 91,353 adults randomly selected from the Danish general population and 187 patients from the Danish α 1 -Antitrypsin Deficiency Registry and recorded baseline blood pressure, baseline plasma lipids and cardiovascular events during follow-up. 185 participants carried the ZZ genotype, 207 carried the SZ genotype and 91,148 carried the MM genotype., Results: α 1 -Antitrypsin deficiency was associated with decreases in blood pressure of up to 5 mmHg for systolic blood pressure and up to 2 mmHg for diastolic blood pressure, in ZZ vs SZ vs MM individuals (trend test, P's ≤ 0.01). Plasma triglycerides and remnant cholesterol were reduced in ZZ individuals compared with MM individuals (t-test, P's < 0.001). α 1 -Antitrypsin deficiency was associated with lower risk of myocardial infarction (trend test P = 0.03), but not with ischemic heart disease, ischemic cerebrovascular disease or hypertension (trend test, P's ≥ 0.59). However, when results for ischemic heart disease were summarized in meta-analysis with results from four previous studies, individuals with versus without α 1 -antitrypsin deficiency had an odds ratio for ischemic heart disease of 0.66 (95% CI:0.53-0.84)., Conclusions: Individuals with severe α 1 -antitrypsin deficiency have lower systolic and diastolic blood pressure, lower plasma triglycerides and remnant cholesterol, reduced risk of myocardial infarction, and a 34% reduced risk of ischemic heart disease., (© 2022. The Author(s).)

Background: SP-D is an important host defense lectin in innate immunity and SP-D deficient mice show several abnormal immune effects and are susceptible to allergen-induced airway disease. At the same time, host microbiome interactions play an important role in the development of allergic airway disease, and alterations to gut microbiota have been linked to airway disease through the gut-lung axis. Currently, it is unknown if the genotype ( Sftpd-/- or Sftpd+/+ ) of the standard SP-D mouse model can affect the host microbiota to such an degree that it would overcome the cohousing effect on microbiota and interfere with the interpretation of immunological data from the model. Generally, little is known about the effect of the SP-D protein in itself and in combination with airway disease on the microbiota. In this study, we tested the hypothesis that microbiome composition would change with the lack of SP-D protein and presence of allergic airway disease in the widely used SP-D-deficient mouse model., Results: We describe here for the first time the lung and gut microbiota of the SP-D mouse model with OVA induced allergic airway disease. After the challenge animals were killed and fecal samples were taken from the caecum and lungs were subjected to bronchoalveolar lavage for comparison of gut and lung microbiota by Illumina 16S rRNA gene sequencing. A significant community shift was observed in gut microbiota after challenge with OVA. However, the microbial communities were not significantly different between SP-D deficient and wild type mice from the same cages in either naïve or OVA treated animals. Wild type animals did however show the largest variation between mice., Conclusions: Our results show that the composition of the microbiota is not influenced by the SP-D deficient genotype under naïve or OVA induced airway disease. However, OVA sensitization and pulmonary challenge did alter the gut microbiota, supporting a bidirectional lung-gut crosstalk. Future mechanistic investigations of the influence of induced allergic airway disease on gut microbiota are warranted.

Conventional identification of Aeromonas species based on biochemical methods is challenged by the heterogeneous nature of the species. Here, we present a new multiplex PCR method directed toward the gyrB and rpoB genes that identifies four Aeromonas species, A. hydrophila, A. media, A. veronii, and A. caviae, and we describe the application of this method on a Danish strain collection., (Copyright © 2015, American Society for Microbiology. All Rights Reserved.)