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Alcohol-induced adipose tissue macrophage phenotypic switching is independent of myeloid Toll-like receptor 4 expression.
Fulham, Melissa A; Ratna, Anuradha; Gerstein, Rachel M; Kurt-Jones, Evelyn A; Mandrekar, Pranoti.
Afiliação
  • Fulham MA; Graduate School of Biomedical Sciences, University of Massachusetts Medical School, Worcester, Massachusetts.
  • Ratna A; Division of Gastroenterology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts.
  • Gerstein RM; Division of Gastroenterology, Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts.
  • Kurt-Jones EA; Program in Innate Immunity, University of Massachusetts Medical School, Worcester, Massachusetts.
  • Mandrekar P; Department of Microbiology and Physiological Systems, University of Massachusetts Medical School, Worcester, Massachusetts.
Am J Physiol Cell Physiol ; 317(4): C687-C700, 2019 10 01.
Article em En | MEDLINE | ID: mdl-31268779
Alcoholic liver disease results from a combination of immune and metabolic pathogenic events. In addition to liver injury, chronic alcohol consumption also causes adipose tissue inflammation. The specific immune mechanisms that drive this process are unknown. Here, we sought to determine the role of the innate immune receptor Toll-like receptor 4 (TLR4) in alcohol-induced adipose tissue inflammation. Using a model of chronic, multiple-binge alcohol exposure, we showed that alcohol-mediated accumulation of proinflammatory adipose tissue macrophages was absent in global TLR4 knockout mice. Proinflammatory macrophage accumulation did not depend on macrophage TLR4 expression; LysMCre-driven deletion of Tlr4 from myeloid cells did not affect circulating endotoxin or the accumulation of M1 macrophages in adipose tissue following alcohol exposure. Proinflammatory cytokine/chemokine production in the adipose stromal vascular fraction also occurred independently of TLR4. Finally, the levels of other adipose immune cells, such as dendritic cells, neutrophils, B cells, and T cells, were modulated by chronic, multiple-binge alcohol and the presence of TLR4. Together, these data indicate that TLR4 expression on cells, other than myeloid cells, is important for the alcohol-induced increase in proinflammatory adipose tissue macrophages.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Tecido Adiposo / Adipócitos / Etanol / Receptor 4 Toll-Like / Macrófagos Limite: Animals Idioma: En Revista: Am J Physiol Cell Physiol Assunto da revista: FISIOLOGIA Ano de publicação: 2019 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Tecido Adiposo / Adipócitos / Etanol / Receptor 4 Toll-Like / Macrófagos Limite: Animals Idioma: En Revista: Am J Physiol Cell Physiol Assunto da revista: FISIOLOGIA Ano de publicação: 2019 Tipo de documento: Article