Neisseria species as pathobionts in bronchiectasis

Li, Liang; Aogáin, Micheál Mac; Xu, Tengfei; Jaggi, Tavleen Kaur; Chan, Louisa; Qu, Jing; Wei, Lan; Liao, Shumin; Cheng, Hong Sheng; Keir, Holly R.; Dicker, Alison; Tan, Kai Sen; Wang, Yun; Koh, Mariko Siyue; Ong, Thun How; Lim, Albert Yick Hou; Abisheganaden, John; Low, Teck Boon; Hassan, Tidi; Long, Xiang; Wark, Peter; Oliver, Brian; Drautz–Moses, Daniela I.; Schuster, Stephan C.; Tan, Nguan Soon; Fang, Mingliang; Chalmers, James D.; Chotirmall, Sanjay H.

doi:10.1016/j.chom.2022.08.005

Cited by 28 publications

(35 citation statements)

References 85 publications

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“…Earlier studies demonstrated the tissue-damaging effects of bacterial infection with non-typable H. influenzae using models of nasal turbinate epithelium ( 244 ). Similar observations have been recently reported for N. subflava ( 9 ). In dysbiosis, bacterial components such as lipoproteins, lipopolysaccharide, and peptidoglycans are released, inducing innate immune responses.…”

Section: Microbe-host Immune Interactionssupporting

confidence: 92%

“…The induction of M1/M2 macrophage phenotypes results in a mixed phenotype of airway inflammation and tissue damage driven by classical (i.e., M1) phenotype and airway remodeling and fibrosis driven by alternative (i.e., M2) phenotype. Similar to smoke-induced COPD, other studies report a gradual transition from upregulation of M1 genes to downregulation of the same genes followed by upregulation of M2-related genes ( 9 , 392 ), which is usually a typical pattern followed from acute inflammation to resolution. Chronic inflammation driven by dysbiosis with a resultant mixed M1/M2 phenotype is the most likely occurrence.…”

Section: Macrophages and The Microbiomementioning

confidence: 79%

“…Compared with controls, alveolar macrophages obtained from microbiome-depleted mice showed a diminished capacity to phagocytose bacteria ( 389 ). In dysbiosis, pathobionts directly infect alveolar macrophages and use them as vehicles to access the lung interstitium ( Figures 3 , 4 ), attracting neutrophils, monocytes, and other inflammatory cells to orchestrate inflammation and lung damage ( 9 , 390 ). In dysbiosis, the airway microenvironment drives the activation of alveolar macrophages, resulting in mixed phenotypes observed in COPD ( 391 ).…”

Section: Macrophages and The Microbiomementioning

confidence: 99%

“…However, it is still unclear how changes in airway microbiota drive persistent immune activation and consequent lung damage in COPD. Whereas N. subflava has been recently demonstrated to drive bronchiectasis, only indirect inference is presently possible for COPD (9,10). Because of the existence of a well-documented overlap between COPD and bronchiectasis (11)(12)(13)(14)(15), it is plausible that N. subflava could contribute to COPD pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

“…Following the publication of early reports in 2010 describing the lung microbiome ( 112 – 115 ), authors revised the vicious circle to suggest that insults such as tobacco smoke exposure, which impair airway mucosal defenses mediate dysbiosis, leading to dysregulated immune response, further impairment of mucosal defense and ensuing dysbiosis, inducing inflammation and further dysbiosis ( 99 ). In distal airways, this inflammation contributes to tissue damage and progressive obstruction, as is the case for P. aeruginosa and N. subflava ( 9 , 116 , 117 ). These effects are mediated via the release of bacterial outer membrane vesicles harboring extracellular products, such as LPS, a potent inflammatory stimulus demonstrated by earlier studies to induce lung emphysema in hamsters ( 118 ).…”

Section: Introductionmentioning

confidence: 99%

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Airway microbiome-immune crosstalk in chronic obstructive pulmonary disease

et al. 2023

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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.

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Section: Microbe-host Immune Interactionssupporting

confidence: 92%

Section: Macrophages and The Microbiomementioning

confidence: 79%

Section: Macrophages and The Microbiomementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Airway microbiome-immune crosstalk in chronic obstructive pulmonary disease

et al. 2023

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Environmental exposure, airway microbiome and respiratory health: You are what you breathe

Yi,

Cai,

Gao

et al. 2023

Clinical & Translational Med

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Our human respiratory system is constantly exposed to the stimuli of environmental toxicants, which is known to trigger a dysregulated lung immune response and lead to respiratory symptoms, impaired lung function and development of respiratory diseases. 1,2 Mounting evidence suggests the existence of a microbial community or microbiome, composing of bacteria, fungi, and viruses, in healthy human lungs, which plays an indispensable role in respiratory health and diseases. 3,4 Nevertheless, it remains unclear how the airway microbial ecosystem responds to environmental exposure and whether it is implicated in the exposure's effects on respiratory health. Through a population-based microbiome survey in Guangdong province, China, we have recently showed that the airway microbiome not only mediates the effects of environmental exposure on respiratory health, but also may impact an individual's susceptibility to exposure (Figure 1), thereby could be a promising new source of biomarkers and targets for environmental risk evaluation and prevention. 5 THE POPULATION-BASED AIRWAY MICROBIOME SURVEYDespite extensive studies on the airway microbiome in patients with respiratory diseases, characterization of the This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

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A lung pathobiont story: Thinking outside the Koch’s postulate box

Singh

2022

Cell Host & Microbe

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Neisseria species as pathobionts in bronchiectasis

Cited by 28 publications

References 85 publications

Airway microbiome-immune crosstalk in chronic obstructive pulmonary disease

Airway microbiome-immune crosstalk in chronic obstructive pulmonary disease

Environmental exposure, airway microbiome and respiratory health: You are what you breathe

A lung pathobiont story: Thinking outside the Koch’s postulate box

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