PM2.5 impairs macrophage functions to exacerbate pneumococcus-induced pulmonary pathogenesis.
Part Fibre Toxicol
; 17(1): 37, 2020 08 04.
Article
in En
| MEDLINE
| ID: mdl-32753046
ABSTRACT
BACKGROUND:
Pneumococcus is one of the most common human airway pathogens that causes life-threatening infections. Ambient fine particulate matter (PM) with aerodynamic diameter ≤ 2.5 µm (PM2.5) is known to significantly contribute to respiratory diseases. PM2.5-induced airway inflammation may decrease innate immune defenses against bacterial infection. However, there is currently limited information available regarding the effect of PM2.5 exposure on molecular interactions between pneumococcus and macrophages.RESULTS:
PM2.5 exposure hampered macrophage functions, including phagocytosis and proinflammatory cytokine production, in response to pneumococcal infection. In a PM2.5-exposed pneumococcus-infected mouse model, PM2.5 subverted the pulmonary immune response and caused leukocyte infiltration. Further, PM2.5 exposure suppressed the levels of CXCL10 and its receptor, CXCR3, by inhibiting the PI3K/Akt and MAPK pathways.CONCLUSIONS:
The effect of PM2.5 exposure on macrophage activity enhances pneumococcal infectivity and aggravates pulmonary pathogenesis.Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Air Pollutants
/
Particulate Matter
/
Lung
Type of study:
Etiology_studies
Limits:
Animals
/
Humans
Language:
En
Journal:
Part Fibre Toxicol
Journal subject:
TOXICOLOGIA
Year:
2020
Document type:
Article
Affiliation country: