Journal article

TNFRp75-dependent immune regulation of alveolar macrophages and neutrophils during early Mycobacterium tuberculosis and Mycobacterium bovis BCG infection


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Publication Details

Author list: Walters A, Keeton R, Labuschagné A, Hsu N, Jacobs M

Publisher: Wiley: 12 months

Publication year: 2021

Journal: Immunology

Journal name: Immunology

Volume number: 162

Issue number: 2

Start page: 220

End page: 234

Total number of pages: 15

ISBN: 13652567 00192805

ISSN: 0019-2805

eISSN: 1365-2567

URL: http://www.scopus.com/inward/record.url?eid=2-s2.0-85093512603&partnerID=MN8TOARS


Abstract

TNF signalling through TNFRp55 and TNFRp75, and receptor shedding is important for immune activation and regulation. TNFRp75 deficiency leads to improved control of Mycobacterium tuberculosis (M. tuberculosis) infection but the effects of early innate immune events in this process are unclear. We investigated the role of TNFRp75 on cell activation and apoptosis of alveolar macrophages and neutrophils during M. tuberculosis and M. bovis BCG infection. We found increased microbicidal activity against M. tuberculosis occurred independently of IFNy and NO generation, and displayed an inverse correlation with alveolar macrophages (AMs) apoptosis. Both M. tuberculosis and M. bovis BCG induced higher expression of MHC-II in TNFRp75-/- AMs, however M bovis BCG infection did not alter AM apoptosis in the absence of TNFRp75. Pulmonary concentrations of CCL2, CCL3 and IL-1β were increased in TNFRp75-/- mice during M, bovis BCG infection, but had no effect on neutrophil responses. Thus, TNFRp75 dependent regulation of mycobacterial replication is virulence dependent and occurs independently of early alveolar macrophage apoptosis and neutrophil responses.


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Last updated on 2021-23-02 at 21:04