作者
Ruth Zomuansangi,C. Lalbiaktluangi,Vijai Kumar Gupta,Austin A. Medders,Jorge E. Vidal,Bhim Pratap Singh,Jae-Jun Song,Prashant Kumar Singh,Amitabh Singh,Balachandar Vellingiri,Mahalaxmi Iyer,Mukesh Yadav
摘要
Air pollution is a major global health issue and a significant risk factor for respiratory infections. Air pollution containing inhalable particulate matter (PM), including Diesel Exhaust Particles (DEP), Urban Particles (UP), tobacco smoke particles, dust particles, ambient Black Carbon (BC), household smoke, etc., emitted from vehicles, industry, construction, agriculture waste burning, cooking, etc., exerts a negative effect on human health. The exposure of inhalable PM to the upper airways, often colonized by opportunistic microbes, represents a unique risk for respiratory infections. Several epidemiological studies reported that PM exposure increases susceptibility to, and severity of, lower respiratory infections like pneumonia or other important diseases such as otitis media, asthma, lung cancer, cardiovascular disease, and Chronic Obstructive Pulmonary disease (COPD). It has been suggested that inhalable PM exposure damages airway epithelial cells, alters the immune response, affects the microbiota, and, as a result, opportunist or pathogenic bacteria (Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, Pseudomonas aeruginosa, or Staphylococcus aureus) establishes respiratory infections. PM and bacteria interaction alters bacteria physiology and enhances bacterial proliferation and biofilm mode of growth. However, the exact mechanism pertaining to how the PM reverts the opportunistic bacteria of the nasopharynx to a pathogenic state is not well understood. In the present review, we have focused on understanding the airborne PM and bacteria interaction that makes humans more susceptible to otherwise harmless bacteria, especially those in the upper airways. Further, we have provided an overview of potential mechanisms triggered by air pollutants to induce bacterial infectious diseases.