Mycobacterium abscessus and M. avium trigger Toll-like receptor 2 and distinct cytokine response in human cells

dc.creatorSampaio, Elizabeth P.
dc.creatorElloumi, Houda Z.
dc.creatorZelazny, Adrian
dc.creatorDing, Li
dc.creatorPaulson, Michelle L.
dc.creatorSher, Alan
dc.creatorBafica, Andre L.
dc.creatorShea, Yvonne R.
dc.creatorHolland, Steven M.
dc.date2019-04-02T13:49:16Z
dc.date2019-04-02T13:49:16Z
dc.date2008
dc.date.accessioned2023-09-26T22:16:28Z
dc.date.available2023-09-26T22:16:28Z
dc.identifierSAMPAIO, Elizabeth P. et al. Mycobacterium abscessus and M. avium Trigger Toll-Like Receptor 2 and Distinct Cytokine Response in Human Cells. American Journal of Respiratory Cell and Molecular Biology, v. 39. p. 431–439, 2008.
dc.identifier1044-1549
dc.identifierhttps://www.arca.fiocruz.br/handle/icict/32327
dc.identifier10.1165/rcmb.2007-0413OC
dc.identifier1535-4989
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/8877158
dc.descriptionMycobacterium 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.
dc.formatapplication/pdf
dc.languageeng
dc.publisherAmerican Thoracic Society
dc.rightsopen access
dc.subjectFator de necrose tumoral-a
dc.subjectQuimiocinas
dc.subjectReceptor 2 Toll-Like
dc.subjectMycobacterium avium
dc.subjectM. abscessus
dc.subjectTumor necrosis factor-a
dc.subjectM. abscessus
dc.subjectM. avium
dc.subjectChemokines
dc.subjectToll-like receptor 2
dc.subjectReceptor 2 Toll-Like
dc.titleMycobacterium abscessus and M. avium trigger Toll-like receptor 2 and distinct cytokine response in human cells
dc.typeArticle


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