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

Myeloid HIF-1α regulates pulmonary inflammation during experimental Mycobacterium tuberculosis infection. Immunology. 2019 Oct 13;: Authors: Resende M, Ferreira CM, Barbosa AM, Cardoso MS, Sousa J, Saraiva M, Castro AG, Appelberg R, Torrado E Abstract The transcription factor hypoxia inducible factor-1 alpha (HIF-1α) is as key regulator of the response and function of myeloid cells in hypoxic and inflammatory microenvironments. To define the role of HIF-1α in tuberculosis, the progression of aerosol Mycobacterium tuberculosis infection was analyzed in mice deficient in HIF-1α in the myeloid lineage (mHIF-1α-/- ). We show that myeloid HIF-1α is not required for the containment of the infection, as both WT and mHIF-1α-/- mice mounted normal Th1 responses and maintained control of bacterial growth throughout infection. However, during chronic infection mHIF-1α-/- mice developed extensive lymphocytic inflammatory involvement of the interstitial lung tissue and died earlier than WT mice. These data support the hypothesis that HIF-1α activity coordinates the response of myeloid cells during M. tuberculosis infection to prevent excessive leukocyte recruitment and immunopathological consequences to the host. PMID: 31606895 [PubMed - as supplied by publisher]
Source: Immunology - Category: Allergy & Immunology Authors: Tags: Immunology Source Type: research