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

• Tipo: Artigo em Revista Científica Internacional
• Data: 2020

Autores

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

Revista

Título: Immunology

Vol. 159

Páginas: 121-129

ISSN: 0019-2805

Editora: Wiley-Blackwell

Indexação

ISI Web of Knowledge - 1 Citação

Scopus - 6 Citações

Outras Informações

ID Authenticus: 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.

Idioma: Inglês

Tipo (Avaliação Docente): Científica

Nº de páginas: 9