2018
DOI: 10.1016/j.cimid.2018.06.005
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Mycobacterium avium complex infection in pigs: A review

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Cited by 18 publications
(12 citation statements)
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“…This interaction leads to phagocytosis and the release of reactive metabolites, resulting in the initiation of intracellular signaling and the release of cytokines and MACs employ several mechanisms to survive in adverse conditions inside macrophages: they produce agents that inhibit the mechanisms associated with an oxidative burst (e.g. superoxide dismutase or heat shock proteins), or inhibit the fusion of phagosome and lysosome [42]. The recognition of MAC by macrophages mainly acts through toll-like receptor 2 (TLR2) [43]; this leads to the production of pro-inflammatory cytokines, such as interleukins IL-1β, IL-12, IL-18, tumour necrosis factor α (TNFα), as well as chemokines such as the C-X-C motif chemokine 10 (CXCL-10) [42].…”
Section: Pathogenesis and Immunology Of Infection The Exact Pathogenesis Of Mac Infections And Their Virulence Factorsmentioning
confidence: 99%
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“…This interaction leads to phagocytosis and the release of reactive metabolites, resulting in the initiation of intracellular signaling and the release of cytokines and MACs employ several mechanisms to survive in adverse conditions inside macrophages: they produce agents that inhibit the mechanisms associated with an oxidative burst (e.g. superoxide dismutase or heat shock proteins), or inhibit the fusion of phagosome and lysosome [42]. The recognition of MAC by macrophages mainly acts through toll-like receptor 2 (TLR2) [43]; this leads to the production of pro-inflammatory cytokines, such as interleukins IL-1β, IL-12, IL-18, tumour necrosis factor α (TNFα), as well as chemokines such as the C-X-C motif chemokine 10 (CXCL-10) [42].…”
Section: Pathogenesis and Immunology Of Infection The Exact Pathogenesis Of Mac Infections And Their Virulence Factorsmentioning
confidence: 99%
“…superoxide dismutase or heat shock proteins), or inhibit the fusion of phagosome and lysosome [42]. The recognition of MAC by macrophages mainly acts through toll-like receptor 2 (TLR2) [43]; this leads to the production of pro-inflammatory cytokines, such as interleukins IL-1β, IL-12, IL-18, tumour necrosis factor α (TNFα), as well as chemokines such as the C-X-C motif chemokine 10 (CXCL-10) [42]. Chemokines and TNFα cause taxis of inflammatory cells such as lymphocytes, macrophages and dendritic cells, to the inflammation site.…”
Section: Pathogenesis and Immunology Of Infection The Exact Pathogenesis Of Mac Infections And Their Virulence Factorsmentioning
confidence: 99%
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