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Dectin-1-Independent Macrophage Phagocytosis of Mycobacterium abscessus.
Ochoa, Alma E; Congel, Jack H; Corley, Jodi M; Janssen, William J; Nick, Jerry A; Malcolm, Kenneth C; Hisert, Katherine B.
Afiliação
  • Ochoa AE; Department of Medicine, National Jewish Health, 1400 Jackson Street, Room A550, Denver, CO 80206, USA.
  • Congel JH; Department of Medicine, National Jewish Health, 1400 Jackson Street, Room A550, Denver, CO 80206, USA.
  • Corley JM; Department of Medicine, National Jewish Health, 1400 Jackson Street, Room A550, Denver, CO 80206, USA.
  • Janssen WJ; Department of Medicine, National Jewish Health, 1400 Jackson Street, Room A550, Denver, CO 80206, USA.
  • Nick JA; Department of Medicine, National Jewish Health, 1400 Jackson Street, Room A550, Denver, CO 80206, USA.
  • Malcolm KC; Department of Medicine, National Jewish Health, 1400 Jackson Street, Room A550, Denver, CO 80206, USA.
  • Hisert KB; Department of Medicine, National Jewish Health, 1400 Jackson Street, Room A550, Denver, CO 80206, USA.
Int J Mol Sci ; 24(13)2023 Jul 04.
Article em En | MEDLINE | ID: mdl-37446240
ABSTRACT
Mycobacterium abscessus, a species of nontuberculous mycobacteria (NTM), is an opportunistic pathogen that is readily cleared by healthy lungs but can cause pulmonary infections in people with chronic airway diseases. Although knowledge pertaining to molecular mechanisms of host defense against NTM is increasing, macrophage receptors that recognize M. abscessus remain poorly defined. Dectin-1, a C-type lectin receptor identified as a fungal receptor, has been shown to be a pathogen recognition receptor (PRR) for both M. tuberculosis and NTM. To better understand the role of Dectin-1 in host defense against M. abscessus, we tested whether blocking Dectin-1 impaired the uptake of M. abscessus by human macrophages, and we compared M. abscessus pulmonary infection in Dectin-1-deficient and wild-type mice. Blocking antibody for Dectin-1 did not reduce macrophage phagocytosis of M. abscessus, but did reduce the ingestion of the fungal antigen zymosan. Laminarin, a glucan that blocks Dectin-1 and other PRRs, caused decreased phagocytosis of both M. abscessus and zymosan. Dectin-1-/- mice exhibited no defects in the control of M. abscessus infection, and no differences were detected in immune cell populations between wild type and Dectin-1-/- mice. These data demonstrate that murine defense against M. abscessus pulmonary infection, as well as ingestion of M. abscessus by human macrophages, can occur independent of Dectin-1. Thus, additional PRR(s) recognized by laminarin participate in macrophage phagocytosis of M. abscessus.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Mycobacterium abscessus / Infecções por Mycobacterium não Tuberculosas Limite: Animals / Humans Idioma: En Ano de publicação: 2023 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Mycobacterium abscessus / Infecções por Mycobacterium não Tuberculosas Limite: Animals / Humans Idioma: En Ano de publicação: 2023 Tipo de documento: Article