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Deficiency of interleukin-6 receptor ameliorates PM2.5 exposure-induced pulmonary dysfunction and inflammation but not abnormalities in glucose homeostasis.
- Source :
- Ecotoxicology & Environmental Safety; Dec2022, Vol. 247, pN.PAG-N.PAG, 1p
- Publication Year :
- 2022
-
Abstract
- Ambient fine particulate matter (PM 2.5) exposure increases local and systemic interleukin-6 (IL-6). However, the pathogenic role of IL-6 signalling following PM 2.5 exposure, particularly in the development of pulmonary dysfunction and abnormal glucose homeostasis, has hardly been investigated. In the study, IL-6 receptor (IL-6R)-deficient (IL-6R<superscript>-/-</superscript>) and wildtype littermate (IL-6R<superscript>+/+</superscript>) mice were exposed to concentrated ambient PM 2.5 (CAP) or filtered air (FA), and their pulmonary and metabolic responses to these exposures were analyzed. Our results demonstrated that IL-6R deficiency markedly alleviated PM 2.5 exposure-induced increases in lung inflammatory markers including the inflammation score of histological analysis, the number of macrophages in bronchoalveolar lavage fluid (BALF), and mRNA expressions of TNFα, IL-1β and IL-6 and abnormalities in lung function test. However, IL-6R deficiency did not reduce the hepatic insulin resistance nor systemic glucose intolerance and insulin resistance induced by PM 2.5 exposure. Our findings support the crucial role of IL-6 signalling in the development of pulmonary inflammation and dysfunction due to PM 2.5 exposure but question the putative central role of pulmonary inflammation for the extra-pulmonary dysfunctions following PM 2.5 exposure, providing a deep mechanistic insight into the pathogenesis caused by PM 2.5 exposure. [Display omitted] • IL-6R deficiency alleviates PM 2.5 exposure-induced pulmonary dysfunction. • IL-6R deficiency aggravates PM 2.5 -induced glucose intolerance and insulin resistance. • PM 2.5 induces adipose hypertrophy and inflammation in WT and IL-6R deficient mice. • IL-6R deficiency reduces PM 2.5 -induced pulmonary but not extra-pulmonary inflammation. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 01476513
- Volume :
- 247
- Database :
- Supplemental Index
- Journal :
- Ecotoxicology & Environmental Safety
- Publication Type :
- Academic Journal
- Accession number :
- 160238697
- Full Text :
- https://doi.org/10.1016/j.ecoenv.2022.114253