| First Author | Resende M | Year | 2020 |
| Journal | Immunology | Volume | 159 |
| Issue | 1 | Pages | 121-129 |
| PubMed ID | 31606895 | Mgi Jnum | J:286253 |
| Mgi Id | MGI:6394172 | Doi | 10.1111/imm.13131 |
| Citation | Resende M, et al. (2020) Myeloid HIF-1alpha regulates pulmonary inflammation during experimental Mycobacterium tuberculosis infection. Immunology 159(1):121-129 |
| abstractText | The transcription factor hypoxia-inducible factor-1 alpha (HIF-1alpha) is a key regulator of the response and function of myeloid cells in hypoxic and inflammatory microenvironments. To define the role of HIF-1alpha in tuberculosis, the progression of aerosol Mycobacterium tuberculosis infection was analysed in mice deficient in HIF-1alpha in the myeloid lineage (mHIF-1alpha(-/-) ). We show that myeloid HIF-1alpha is not required for the containment of the infection, as both wild-type (WT) and mHIF-1alpha(-/-) mice mounted normal Th1 responses and maintained control of bacterial growth throughout infection. However, during chronic infection mHIF-1alpha(-/-) mice developed extensive lymphocytic inflammatory involvement of the interstitial lung tissue and died earlier than WT mice. These data support the hypothesis that HIF-1alpha activity coordinates the response of myeloid cells during M. tuberculosis infection to prevent excessive leucocyte recruitment and immunopathological consequences to the host. |
