Please use this identifier to cite or link to this item: https://www.arca.fiocruz.br/handle/icict/39927
Title: Mycobacterium abscessus and M. avium trigger Toll-like receptor 2 and distinct cytokine response in human cells
Authors: Sampaio, Elizabeth P.
Elloumi, Houda Z.
Zelazny, Adrian
Ding, Li
Paulson, Michelle L.
Sher, Alan
Bafica, Andre L.
Shea, Yvonne R.
Holland, Steven M.
Affilliation: National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Bethesda, Maryland, USA / Fundação Oswaldo Cruz. Instituto Oswaldo Cruz. Laboratório de Hanseníase. Rio de Janeiro, RJ, Brasil.
National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Bethesda, Maryland, USA.
National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Bethesda, Maryland, USA.
National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Bethesda, Maryland, USA.
National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Bethesda, Maryland, USA
National Institute of Allergy and Infectious Diseases. Laboratory of Parasitic Diseases. Immunobiology Section. Bethesda, Maryland, USA.
National Institute of Allergy and Infectious Diseases. Laboratory of Parasitic Diseases. Immunobiology Section. Bethesda, Maryland, USA.
National Institute of Allergy and Infectious Diseases. Clinical Center. Department of Laboratory Medicine. Bethesda, Maryland, USA.
National Institute of Allergy and Infectious Diseases. Laboratory of Clinical Infectious Diseases. Bethesda, Maryland, USA.
Abstract: Mycobacterium avium (MAV) and M. abscessus (MAB) are ubiquitous environmental organisms increasingly recognized to cause chronic lung disease in patients with apparently normal immune function. Little is yet known about their human pathophysiology. Our objective was to examine cytokine and chemokine responses (protein and gene expression) and signaling pathways triggered by reference and clinical isolates of MAB and MAV in human peripheral blood mononuclear cells, monocytes, and murine bone marrow-derived macrophages in vitro. MAB-induced TNF-alpha production was higher than that induced by MAV. IFN-gamma, IL-1beta, and the chemokines macrophage inflammatory protein-1alpha and regulated on activation, normal T cell expressed and secreted were equally up-regulated. Differences between MAB and MAV do not require replication and are heat stable. We found no differential effect due to rough or smooth colonies within the same species. Similar to MAV, MAB triggered mitogen-activated protein kinase (MAPK) signaling and nuclear factor-kappaB translocation. Induction of TNF-alpha was dependent on MAPK pathways, since pre-incubation of cells with signaling inhibitors led to more than 85% reduction in cytokine secretion. MAB also triggered a Toll-like receptor 2 (TLR2)-mediated response that led to TNF-alpha production by human monocytes. Accordingly, stimulation of murine TLR2- or myeloid differentiation factor 88-deficient bone marrow-derived macrophages did not elicit TNF-alpha, reinforcing a critical role for TLR2 in MAB-induced cell activation. We concluded that MAB signals human cells through MAPK and TLR2 pathways and triggers more pronounced pro-inflammatory cytokines and chemokines than MAV.
Keywords: Tumor necrosis factor-a
M. abscessus
M. avium
Chemokines
Toll-like receptor 2
keywords: M. abscessus
M. avium
Quimiocinas
Fator de necrose tumoral 2
Receptores Toll-Like
DeCS: Receptores Toll-Like
Issue Date: 2008
Publisher: American Thoracic Society
Citation: SAMPAIO, Elizabeth P. et al. Mycobacterium abscessus and M. avium Trigger Toll-Like Receptor 2 and Distinct Cytokine Response in Human Cells. Am J Respir Cell Mol Biol., v. 39, p. 431-439, Apr. 2008.
DOI: 10.1165/rcmb.2007-0413OC
ISSN: 1044-1549
Copyright: open access
Appears in Collections:IOC - Artigos de Periódicos

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