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  • Title: Myeloid HIF-1α regulates pulmonary inflammation during experimental Mycobacterium tuberculosis infection.
    Author: Resende M, Ferreira CM, Barbosa AM, Cardoso MS, Sousa J, Saraiva M, Castro AG, Appelberg R, Torrado E.
    Journal: Immunology; 2020 Jan; 159(1):121-129. PubMed ID: 31606895.
    Abstract:
    The transcription factor hypoxia-inducible factor-1 alpha (HIF-1α) is a 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 analysed 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 wild-type (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 leucocyte recruitment and immunopathological consequences to the host.
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