The tobacco industry promotes electronic nicotine delivery systems (ENDS) and heated tobacco products (HTP) as a safer alternative to conventional cigarettes with misleading marketing sustained by studies with conflict of interest. As a result, these devices sell without regulations and warnings about their adverse effects on health, with a growing user base targeting young people. This systematic review aimed to describe the adverse effects on the respiratory system in consumers of these devices. We conducted a systematic review and bibliometric analysis of 79 studies without conflict of interest evaluating ENDS and HTP effects in the respiratory system in experimental models, retrieved from the PubMed database. We found that the damage produced by using these devices is involved in pathways related to pulmonary diseases, involving mechanisms previously reported in conventional cigarettes as well as new mechanisms particular to these devices, which challenges that the tobacco industry’s claims. The present study provides significant evidence to suggest that these devices are an emerging public health problem and that they should be regulated or avoided.

Overproduction of inflammatory cytokines is a keystone event in COVID-19 pathogenesis; TNF and its receptors (TNFR1 and TNFR2) are critical pro-inflammatory molecules. ADAM17 releases the soluble (sol) forms of TNF, TNFR1, and TNFR2. This study evaluated TNF, TNFRs, and ADAM17 at the protein, transcriptional, and gene levels in COVID-19 patients with different levels of disease severity. In total, 102 patients were divided into mild, moderate, and severe condition groups. A group of healthy donors (HD; n = 25) was included. Our data showed that solTNFR1 and solTNFR2 were elevated among the COVID-19 patients (p < 0.0001), without increasing the transcriptional level. Only solTNFR1 was higher in the severe group as compared to the mildly ill (p < 0.01), and the level was higher in COVID-19 patients who died than those that survived (p < 0.0001). The solTNFR1 level had a discrete negative correlation with C-reactive protein (p = 0.006, Rho = −0.33). The solADAM17 level was higher in severe as compared to mild disease conditions (p < 0.01), as well as in COVID-19 patients who died as compared to those that survived (p < 0.001). Additionally, a potential association between polymorphism TNFRSF1A:rs767455 and a severe degree of disease was suggested. These data suggest that solTNFR1 and solADAM17 are increased in severe conditions. solTNFR1 should be considered a potential target in the development of new therapeutic options.

Background: COVID-19 is an infectious disease caused by the severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2). Many COVID-19 patients require invasive mechanical ventilation (IMV) while others, even with acute respiratory failure, do not (NIMV). Therefore, we aimed to evaluate serum levels of MMP-7 and molecules related to exhausted T-cells as potential biomarkers to differentiate between IMV and NIMV patients. Methods: 105 patients diagnosed with COVID-19 and confirmed by RT-PCR for SARS-CoV-2 were divided into two groups according to the requirement for IMV. Serum levels of sPD-L1, sPD-L2, sTIM-3, sGal-9 and sMMP-7 were quantified by ELISA and correlated with clinical data. Twelve patients were followed up after eight months to compare the levels of the biomarkers between acute disease and post-COVID-19. Results: IMV patients experienced a lower PaO₂/FiO₂ (p < 0.0001) and a longer hospital stay (p < 0.0001), and exhibited higher levels of sPD-L1 (p < 0.05), sTIM-3 (p < 0.01) and sMMP-7 (p < 0.0001) when compared with NIMV patients. According to a ROC analysis, sMMP-7 had the highest sensitivity (78%) and specificity (76%) with a cut point of 4.5 ng/mL, followed by sTIM-3 and sPD-L1. Eight months post-COVID-19, IMV patients displayed a significant decrease in the initially high levels of sPD-L1, sTIM-3 and sGal-9, while sPD-L2 was increased, and sMMP-7 was unchanged. Conclusion: Circulating levels of sPD-L1, sTIM-3 and sMMP-7 are potential biomarkers of disease severity to distinguish patients requiring IMV. MMP-7 could also be a marker for the persistence of lung lesions post-COVID-19.

Journal of Medical Internet Research - International Scientific Journal for Medical Research, Information and Communication on the Internet #Preprint #PeerReviewMe: Warning: This is a unreviewed preprint. Readers are warned that the document has not been peer-reviewed by expert/patient reviewers or an academic editor, may contain misleading claims, and is likely to undergo changes before final publication, if accepted, or may have been rejected/withdrawn. Readers with interest and expertise are encouraged to sign up as peer-reviewer, if the paper is within an open peer-review period. Please cite this preprint only for review purposes or for grant applications and CVs (if you are the author). Background: Of the 14.3 million Mexicans who smoke, only a minority take advantage of evidence-based approaches to smoking cessation. Mobile health interventions have the potential to increase the reach of effective cessation interventions in Mexico and other Low- and Middle-Income Countries (LMICs). Objective: To assess an innovative, personalized, and interactive mobile intervention developed for Mexican smokers. Methods: We recruited 40 Mexican smokers to participate in Vive sin Tabaco… ¡Decídete!, a smoking cessation program that uses a tablet-based decision-support software to drive a 12-week text messaging smoking cessation program and pharmacotherapy support. Outcome measures included participant text messaging interactivity with the program, participant satisfaction, and 12-week end-of-treatment abstinence. Results: Average age of participants was 36 years old, primarily male (65%), with at least an undergraduate degree (62.5%). Most participants (95%) smoked daily and were interested in quitting in the next 7 days. As an indicator of participant interactivity, participants sent an average of 21 text messages during the 12-week intervention (SD=17.62). Of the 843 messages that participants sent to the program, only 96 messages (11.3%) used keywords. At 12 weeks, 16 (40%) participants were biochemically verified abstinent using intent-to-treat analysis (87.5% follow-up rate). The majority of participants (84.4%) reported being very satisfied or extremely satisfied with the program. Conclusions: The Vive sin Tabaco… ¡Decídete! smoking cessation mobile intervention was accepted by participants, generated high satisfaction and high text messaging interactivity, and resulted in noteworthy cessation rates at end-of-treatment. This intervention is a promising strategy for smoking cessation in LMICs. Additional testing as a formal randomized clinical trial appears warranted.

Background. The influenza A H1N1/09 pandemic infected a small number of exposed individuals, which suggests the involvement of genetic factors. There are scarce data available on classical HLA class I association with the influenza A H1N1/09 pandemic. Methods. We analyzed the frequency of classical HLA class I alleles and haplotypes in A H1N1/09 influenza in a case-control study including 138 influenza patients (INF-P) and 225 asymptomatic healthy contacts (INF-C) simultaneously recruited. HLA class I typing was performed by high-resolution sequence-based typing method. Results. Our analysis revealed higher frequency of C∗07:02:01, B∗39:06:02, C∗03:02:01, B∗44:03:01, B∗51:01:05, and B∗73:01 (p<0.05; OR = 1.84–9.98) and of two haplotypes—A∗68:01:02-C∗07:02:01 (p=1.05E−05; OR = 23.99) and B∗35:01:01-C∗07:02.01 (p=4.15E−04, OR = 2.15)—in A H1N1/09 influenza subjects. A∗68:01:01 was exclusively present only in the INF-P group (5/138). A decrease in the frequency of C∗03:03:01, A∗11:01:01, B∗39:01:01, A∗24:02:01, C∗03:04:01, B∗51:01:01, and C∗07:01:01 (p<0.05; OR = 0.12–0.52) and of haplotypes A∗02:01:01-B∗35:01:01-C∗04:01:01, A∗24:02:01-B∗35:01:01, B∗39:01:01-C∗07:02:01, and B∗40:02:01-C∗03:04:01 (p<0.05; OR = 0.08–0.22) were observed in INF-P group. Conclusion. Selective classical HLA class I allele and haplotype combinations predispose individuals towards susceptibility or protection against the influenza A H1N1/09 pandemic. This work has significant implications for accessing population transmission risk for A H1N1/09 or a similar strain breakout in the future.

The lung microbiome composition has critical implications in the regulation of innate and adaptive immune responses. Next-generation sequencing techniques have revolutionized the understanding of pulmonary physiology and pathology. Currently, it is clear that the lung is not a sterile place; therefore, the investigation of the participation of the pulmonary microbiome in the presentation, severity, and prognosis of multiple pathologies, such as asthma, chronic obstructive pulmonary disease, and interstitial lung diseases, contributes to a better understanding of the pathophysiology. Dysregulation of microbiota components in the microbiome–host interaction is associated with multiple lung pathologies, severity, and prognosis, making microbiome study a useful tool for the identification of potential therapeutic strategies. This review integrates the findings regarding the activation and regulation of the innate and adaptive immune response pathways according to the microbiome, including microbial patterns that could be characteristic of certain diseases. Further studies are required to verify whether the microbial profile and its metabolites can be used as biomarkers of disease progression or poor prognosis and to identify new therapeutic targets that restore lung dysbiosis safely and effectively.