Myeloid HIF-1 alpha regulates pulmonary inflammation during experimental Mycobacterium tuberculosis infection

• Type: Article in International Scientific Journal
• Date: 2020

Authors

Resende, M (Author) Other; Ferreira, CM (Author) Other; Barbosa, AM (Author) Other; Cardoso, MS (Author) Other; Sousa, J (Author) Other; Saraiva, M (Author) Other; Castro, AG (Author) Other; Appelberg, R (Author) Other; Torrado, E (Author) Other

Journal

Title: Immunology

Vol. 159

Pages: 121-129

ISSN: 0019-2805

Publisher: Wiley-Blackwell

Indexing

ISI Web of Knowledge - 1 Citation

Scopus - 6 Citations

Other information

Authenticus ID: P-00R-C3M

DOI: 10.1111/imm.13131

Abstract (EN): The transcription factor hypoxia-inducible factor-1 alpha (HIF-1 alpha) is a key regulator of the response and function of myeloid cells in hypoxic and inflammatory microenvironments. To define the role of HIF-1 alpha in tuberculosis, the progression of aerosol Mycobacterium tuberculosis infection was analysed in mice deficient in HIF-1 alpha in the myeloid lineage (mHIF-1 alpha(-/-)). We show that myeloid HIF-1 alpha is not required for the containment of the infection, as both wild-type (WT) and mHIF-1 alpha(-/-) mice mounted normal Th1 responses and maintained control of bacterial growth throughout infection. However, during chronic infection mHIF-1 alpha(-/-) mice developed extensive lymphocytic inflammatory involvement of the interstitial lung tissue and died earlier than WT mice. These data support the hypothesis that HIF-1 alpha activity coordinates the response of myeloid cells during M. tuberculosis infection to prevent excessive leucocyte recruitment and immunopathological consequences to the host.

Language: English

Type (Professor's evaluation): Scientific

No. of pages: 9