Airway microbiome-immune crosstalk in chronic obstructive pulmonary disease

Abstract

Chronic Obstructive Pulmonary Disease (COPD) has significantly contributed to global mortality, with three million deaths reported annually. This impact is expected to increase over the next 40 years, with approximately 5 million people predicted to succumb to COPD-related deaths annually. Immune mechanisms driving disease progression have not been fully elucidated. Airway microbiota have been implicated. However, it is still unclear how changes in the airway microbiome drive persistent immune activation and consequent lung damage. Mechanisms mediating microbiome-immune crosstalk in the airways remain unclear. In this review, we examine how dysbiosis mediates airway inflammation in COPD. We give a detailed account of how airway commensal bacteria interact with the mucosal innate and adaptive immune system to regulate immune responses in healthy or diseased airways. Immune-phenotyping airway microbiota could advance COPD immunotherapeutics and identify key open questions that future research must address to further such translation.

Circadian-Coupled Genes Expression and Regulation in HIV-Associated Chronic Obstructive Pulmonary Disease (COPD) and Lung Comorbidities

“…Refs. [17][18][19] report that lung inflammation is a hallmark of COPD, as shown in Figure 1. HIV infection can cause significant changes in pulmonary immune function, which can lead to increased susceptibility to respiratory infections and other lung diseases [20].…”

Recurrence of pulmonary tuberculosis associated with non-specific lung diseases – a current problem in phthisiopneumology

“…Inițial sub acțiunea aeropolutantelor au loc schimbări structurale consecutive a căilor respiratorii a țesutului pulmonar, se dereglează proprietățile reologice a secretului bronșic [7,8,11,30,40]. Aceste dereglări duc la restructurarea epiteliului și hiperplazia elementelor de mucogeneză a căilor respiratorii, ceea ce provoacă dereglarea clirensului mucociliar, micșorarea rezistenței nespecifice naturale, creând condiții favorabile pentru adeziune și colonizare a agentului bacterian [11,41,42,43,44,45].…”

“…Severitatea evoluției recidivei tuberculozei în asociere cu bolile pulmonare nespecifice este condiționată și de prezența altor patologii asociate: alcoolismul cronic, diabetul zaharat, bolile aparatului cardiovascular etc., care conduc și la reducerea calității vieții [43,45,49,53]. În dezvoltarea recidivei tuberculozei pulmonare un rol important îl joacă bolile pulmonare obstructive cronice (BPOC) [11,30,41,42,43]. Totodată TB și BPOC au factori de risc comuni, cum ar fi fumatul și statutul socioeconomic scăzut [4,7].…”

Unraveling the Pathogenesis of Chronic Obstructive Pulmonary Disease in Alpha-1 Antitrypsin Deficiency: Mechanisms, Biomarkers, and Therapeutic Implications

“…Microbiome-derived signals activate alveolar macrophages and dendritic cells, stimulating different immune cellular players to maintain immune barrier function. The diseased airways become dysbiotic, leading to altered microbial diversity and composition, with the ultimate effect of persistent lung inflammation and tissue injury [22].…”