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The present study aimed to identify in patients with severe COVID-19 and acute respiratory distress syndrome (ARDS) the association between rs3804099 and rs3804100 ( TLR2 ) and evaluate the expression of TLR-2 on the cell surface of innate and adaptive cells of patients' carriers of C allele in at least one genetic variant. We genotyped 1018 patients with COVID-19 and ARDS. According to genotype, a subgroup of 12 patients was selected to stimulate peripheral blood mononuclear cells (PBMCs) with spike and LPS + spike. We evaluated soluble molecules in cell culture supernatants. The C allele in TLR2 (rs3804099, rs3804100) is not associated with a risk of severe COVID-19; however, the presence of the C allele (rs3804099 or rs3804100) affects the TLR-2 ability to respond to a spike of SARS-CoV-2 correctly. The reference group (genotype TT) downregulated the frequency of non-switched TLR-2+ B cells in response to spike stimulus; however, the allele's C carriers group is unable to induce this regulation, but they produce high levels of IL-10, IL-6, and TNF-α by an independent pathway of TLR-2. Findings showed that TT genotypes (rs3804099 and rs3804100) affect the non-switched TLR-2+ B cell distribution. Genotype TT (rs3804099 and rs3804100) affects the TLR-2's ability to respond to a spike of SARS-CoV-2. However, the C allele had increased IL-10, IL-6, and TNF-α by stimulation with spike and LPS.

Background: After hospital discharge, post-COVID-19 syndrome has been observed to be associated with impaired diffusing capacity, respiratory muscle strength, and lung imaging abnormalities, in addition to loss of muscle mass/strength, sarcopenia, and obesity impact exercise tolerance, pulmonary functions, and overall prognosis. However, the relationship between lung function and the coexistence of obesity with low muscle strength and sarcopenia in post-COVID-19 patients remains poorly investigated. Therefore, our aim was to evaluate the association between lung function and the coexistence of obesity with dynapenia and sarcopenia in post-COVID-19 syndrome patients., Methods: This cross-sectional study included subjects who were hospitalized due to moderate to severe COVID-19, as confirmed by PCR testing. Subjects who could not be contacted, declined to participate, or died before the follow-up visit were excluded., Results: A total of 711 subjects were evaluated; the mean age was 53.64 ± 13.57 years, 12.4% had normal weight, 12.6% were dynapenic without obesity, 8.3% had sarcopenia, 41.6% had obesity, 21.2% had dynapenic obesity, and 3.8% had sarcopenic obesity. In terms of pulmonary function, the dynapenic subjects showed decreases of -3.45% in FEV 1 , -12.61 cmH2O in MIP, and -12.85 cmH2O in MEP. On the other hand, the sarcopenic subjects showed decreases of -6.14 cmH2O in MIP and -11.64 cmH2O in MEP. The dynapenic obesity group displayed a reduction of -12.13% in PEF., Conclusions: In post-COVID-19 syndrome, dynapenia and sarcopenia-both with and without obesity-have been associated with lower lung function.

Chronic obstructive pulmonary disease (COPD) patients due to biomass exposure (BE-COPD) could be more affected than COPD due to tobacco smoke (TE-COPD) by the coronavirus disease 2019 (COVID-19) pandemic. The aim of this work was to determine the prevalence of COVID-19 in BE-COPD and TE-COPD and if housing conditions, poor attitude, knowledge, and risk perception towards COVID-19, particularly in BE-COPD women, could represent a risk factor for contagion.An 11% prevalence of COVID-19 was found with no significant difference between COPD groups. The BE-COPD group showed poorer socioeconomic status. No significant differences were found to be associated with SARS-CoV-2 infection regarding housing conditions, poor knowledge, attitude, and risk perception towards COVID-19. Living in urban areas and perceiving risk in COVID-19 were significantly associated with increased adherence to sanitary measures and concern of contagion. Around 40% of all patients showed poor risk perception and adherence to sanitary measures towards COVID-19.

Introduction: Lower respiratory tract infections remain the deadliest communicable disease worldwide. The relationship between cardiovascular diseases and viral infections is well known; for example, during the AH1N1 influenza pandemic, many patients developed acute cardiovascular disease. In the SARS-CoV2 pandemic, cardiovascular health has again become a challenge, with early reports showing cardiac damage in these patients., Objective: The study aims to describe the clinical characteristics of COVID-19 patients with an emphasis on cardiovascular compromises, compared with past outbreaks of influenza AH1N1, to identify prognostic factors of severity., Methods: A cross-sectional study of 72 subjects with a confirmed diagnosis of COVID-19 was conducted. Subjects were evaluated in two groups: 38 hospitalized patients and 34 patients in the Intensive Care Unit (ICU). Data from different outbreaks of influenza AH1N1 were then compared with this group., Results: The 34 subjects in the ICU had higher levels of high sensible troponin, D dimer, creatinine, and leukocytes compared with the 38 hospitalized subjects. The lymphocytes count was diminished in 85.29% of ICU subjects. When compared with AH1N1 patients, it was found that SARS-CoV2 patients were 10 years older on average. The proportion of overweight and obese SARS-CoV2 patients was double that in the influenza outbreaks. In addition, it was observed that a high number of SARS-CoV2 subjects presented with diabetes mellitus., Conclusion: There were various clinical and severity differences between each of these outbreaks. However, viral respiratory infection diseases such as SARS-CoV2 are a significant risk factor for acute ischemic, functional, and structural cardiovascular complications. The only way to combat this risk is a prevention approach, specifically through vaccines, but also through measures that force drastic changes in health policies to reduce perhaps the worst of pandemics, obesity, and its metabolic consequences., Competing Interests: The authors declare they have no conflict of interest.

IL-17A is an important pro-inflammatory cytokine involved in the inflammatory response in chronic obstructive pulmonary disease (COPD). To evaluate the role played by single nucleotide polymorphisms of IL17A and protein levels in susceptibility to COPD, 1,807 subjects were included in a case-control study; 436 had COPD related to tobacco smoking (COPD-S) and 190 had COPD related to biomass burning (COPD-BB). Six hundred fifty-seven smokers without COPD (SWOC) and 183 biomass burning-exposed subjects (BBES) served as the respective control groups. The CC genotype and C allele of rs8193036 were associated with COPD (COPD-S vs. SWOC: p < 0.05; OR = 3.01, and OR = 1.28, respectively), as well as a recessive model (p < 0.01; OR = 2.91). Significant differences in serum levels were identified between COPD-S vs. SWOC, COPD-S vs. COPD-BB, and SWOC vs. BBES (p < 0.01). By comparing genotypes in the COPD-BB group TT vs. CC and TC vs. CC (p < 0.05), we found lower levels for the CC genotype. Logistic regression analysis by co-variables was performed, keeping the associations between COPD-S vs. SWOC with both polymorphisms evaluated (p < 0.05), as well as in COPD-BB vs. BBES but with a reduced risk of exacerbation (p < 0.05). In conclusion, polymorphisms in IL17A are associated with COPD. Serum levels of IL-17A were higher in smokers with and without COPD.

Heat shock proteins (HSP) genes are a superfamily responsible for encoding highly conserved proteins that are important for antigen presentation, immune response regulation, and cellular housekeeping processes. These proteins can be increased by cellular stress related to pollution, for example, smoke from biomass burning and/or tobacco smoking. Single nucleotide polymorphisms (SNPs) in these genes could affect the levels of their proteins, as well as the susceptibility to developing lung diseases, such as chronic obstructive pulmonary disease (COPD), related to the exposure to environmental factors. Methods: The subjects included were organized into two comparison groups: 1,103 smokers (COPD patients, COPD-S = 360; smokers without COPD, SWOC = 743) and 442 never-smokers who were chronically exposed to biomass smoke (COPD patients, COPD-BS = 244; exposed without COPD, BBES = 198). Eight SNPs in three HSP genes were selected and genotyped: four in HSPA1A , two in HSPA1B , and two in HSPA1L . Sputum expectoration was induced to obtain pulmonary cells and relative quantification of mRNA expression. Subsequently, the intracellular protein levels of total Hsp27, phosphorylated Hsp27 (Hsp27p), Hsp60, and Hsp70 were measured in a sample of 148 individuals selected based on genotypes. Results: In the smokers' group, by a dominant model analysis, we found associations between rs1008438 (CA+AA; p = 0.006, OR = 1.52), rs6457452 (CT+TT; p = 0.000015, OR = 1.99), and rs2763979 (CT+TT; p = 0.007, OR = 1.60) and the risk to COPD. Among those exposed to biomass-burning smoke, only rs1008438 (CA+AA; p < 0.01, OR = 2.84) was associated. Additionally, rs1008438 was associated with disease severity in the COPD-S group (AA; p = 0.02, OR = 2.09). An increase in the relative expression level of HSPA1A was found (12-fold change) in the COPD-BS over the BBES group. Differences in Hsp27 and Hsp60 proteins levels were found (p < 0.05) in the comparison of COPD-S vs. SWOC. Among biomass-burning smoke-exposed subjects, differences in the levels of all proteins (p < 0.05) were detected. Conclusion: SNPs in HSP genes are associated with the risk of COPD and severe forms of the disease. Differences in the intracellular Hsp levels are altered depending on the exposition source., (Copyright © 2020 Ambrocio-Ortiz, Pérez-Rubio, Ramírez-Venegas, Hernández-Zenteno, Del Angel-Pablo, Pérez-Rodríguez, Salazar, Abarca-Rojano and Falfán-Valencia.)

Protease inhibitor S (PiS) and protease inhibitor Z (PiZ) variants in the SERPINA1 gene are the main genetics factors associated with COPD; however, investigations about other polymorphisms are scanty. The aim of this study was to evaluate two missense single nucleotide polymorphisms (SNPs) (rs709932 and rs1303) in the SERPINA1 gene in Mexican mestizo patients with chronic obstructive pulmonary disease (COPD) related to tobacco smoking and biomass-burning exposure. 1700 subjects were genotyped and divided into four groups: COPD related to tobacco smoking (COPD-S, n = 297), COPD related to biomass-burning exposure (COPD-BB, n = 178), smokers without COPD (SWOC, n = 674), and biomass-burning exposed subjects (BBES, n = 551) by real-time PCR. Moreover, the patients' groups were divided according to their exacerbations' frequency. We carried out a haplotype analysis. We did not find differences in allele and genotype frequencies between groups in unadjusted and adjusted analyses, neither with these SNPs and lung function decline. Exacerbations' frequency is not associated with these SNPs. However, we found a haplotype with major alleles (CT) associated with reduced risk for COPD ( p < 0.05). Our analysis reveals that SNPs different from PiS and PiZ (rs709932 and rs1303) in the SERPINA1 gene are not associated with COPD and lung function decline in a Mexican mestizo population. However, a haplotype shaped by both major alleles (CT haplotype) is associated with reduced risk for COPD.

Background: The prognosis in patients with Chronic Obstructive Pulmonary Disease (COPD) depends, in large part, on the frequency of exacerbations. Cardiovascular diseases, including heart failure (HF), are the risk factors for exacerbations. However, the importance of HF type over the exacerbations in COPD patients is unknown., Objective: To determine whether right heart failure (RHF) is an independent risk factor for severe exacerbations in patients with COPD., Methods: A prospective cohort study of 133 patients diagnosed with COPD with a follow-up period from 2010 to 2016. Patients with bronchial hyperreactivity, asthma, or pulmonary embolism were excluded., Results: The mean age was 74.7 ± 8.2 years and 43.6% were men, 69.9% had severe exacerbations during follow-up. Subjects with RHF had lower FEV 1 (50.2 ± 19.9 vs 57.4 ± 16.9, P = .006) and greater incidence of stroke (15.4% vs 1.8%, P = .009) compared to those without RHF. Subjects with RHF were at higher risk of severe exacerbations (HR, 2.46; CI 95%, 1.32-4.58, P = .005) compared to those without RHF after adjusting for confounding variables., Conclusion: In patients with COPD, RHF is an independent risk factor for suffering severe exacerbations., (© 2018 John Wiley & Sons Ltd.)

Background: Chronic obstructive pulmonary disease (COPD) is a chronic inflammatory condition characterized by complex lesions of the lungs and other organs as well as a progressive obstruction of the airway. In COPD patients, heart failure (HF) is associated with worse conditions such as inflammation, arterial stiffness, and increased risk mortality. However, the association of HF, COPD, and stroke are unclear; the examination of the role of HF, especially right HF, about increased risk of stroke in COPD patients has not been studied. We aimed to determine if right HF is a risk factor for stroke in patients with COPD., Materials and Methods: A case-control study of patients with COPD was carried out. The cases were defined as COPD patients with ischemic stroke and control COPD patients without stroke., Results: A total of 162 patients with COPD were analyzed: COPD with stroke (n = 35) and COPD alone (n = 127). COPD patients with right HF were at a greater risk of stroke compared with patients without right HF (odds ratio 3.03, 95% confidence interval 1.13-10.12, p = .044) adjusted for confounding factors., Conclusions: Right HF is an independent risk factor for stroke, probably because of cerebrovascular stasis secondary to congestion of the superior vena cava., (Copyright © 2017 National Stroke Association. Published by Elsevier Inc. All rights reserved.)

Background: Early diagnosis of chronic obstructive pulmonary disease (COPD) remains the main intervention to prevent disease progression. However, conflicting results exist on the utility of two different diagnostic strategies that preclude freely recommending one strategy in favor of the other. Spirometry was used to determine the effectiveness of a symptom-based (case-finding) strategy vs. a screening strategy to detect COPD in smokers., Methods: The case-finding strategy was undertaken during the COPD Day campaign in smokers with respiratory symptoms who were willing to submit to lung function testing. Screening was carried out with smokers attending a smoking cessation program. A short standardized questionnaire on respiratory symptoms along with spirometry were carried out and analyzed for both strategies., Results: We evaluated 2781 smokers (mean pack/years 23.38): 1999 from the case-finding strategy and 782 from the smoking cessation program strategy (SCS). Prevalence of COPD according to the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria was 10.1 and 13.3%, respectively (p < 0.01). With the exception of dyspnea (70.6% vs. 72.5%, p = 0.72), prevalence of symptoms such as cough (61.5 vs. 37, p < 0.001), phlegm (60.4 vs. 38.2, p < 0.001) and wheezing (56.7 vs.15.06, p < 0.001) was higher among smokers from the case-finding strategy. Multivariate logistic regression analysis showed that dyspnea [OR = 2.09 (95% CI 1.41-3.1)] was the only common predictor of COPD after jointly and separately analyzing case-finding and screening strategies., Conclusions: For early diagnosis of COPD in a primary care setting, a screening strategy aimed at all smokers may be more useful than a case-finding strategy., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Background: Chronic obstructive pulmonary disease (COPD) is a progressive disorder characterized by an inflammatory response to cigarette smoke. A disorder in immune regulation contributing to the pathogenesis of COPD has been suggested, however, little is known about the involvement of CD4 (+) T cells. To determine the distribution of different CD4(+) T cell subsets in patients with COPD, current smokers without COPD (CS) and healthy subjects (HS), and its correlation with pulmonary function., Methods: Th1, Th2, Th17 and Treg, subsets, were quantified by flow cytometry in peripheral blood (PB) of 39 patients with COPD, 14 CS and 15 HS. Correlations were assessed with Spearman's rank test. The association between Th17 and lung function was evaluated with a multivariate logistic regression analysis., Results: An increase of Th17 cells (median 9.7% range 0.8-22.5%) was observed in patients with COPD compared with CS (median 2.8% range 0.8-10.6) and HS (median 0.6% range 0.4-1%, p < 0.0001). Th1 and Tregs subsets were also increased in COPD and CS compared to HS. Inverse correlations were found between Th17 with FEV(1)%p r = -0.57 and with FEV(1)/FVC r = -0.60, (p < 0.0001 for both comparison). In addition, increase of Th17 predicted the presence [OR 1.76 (CI 95% 1.25-2.49, p = 0.001)] and severity of airflow limitation [OR 1.13 (CI95% 1.02-1.25, p = 0.02)]., Conclusions: The increase of Th17 response and the lost of balance between CD4(+) T cell subsets, suggest a lack of regulation of the systemic inflammatory response that may contribute to pathogenesis in COPD patients., (Copyright © 2011 Elsevier Ltd. All rights reserved.)