Abstract
Trypanosoma cruzi metacyclic trypomastigotes (MT), but not blood form trypomastigotes (BFT), are highly mucosally infective. We investigated the abilities of MT and BFT to induce inflammation and/or intracellular killing activity within mucosal epithelia. BFT, but not MT, induced marked increases in interleukin-8, GRO-alpha, MCP-1, and nitric oxide production in HeLa and AGS cells, despite similar infectivities. MT may avoid induction of inflammation as an important biological mechanism facilitating mucosal invasion.
MeSH terms
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Animals
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Cell Line
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Chagas Disease / etiology
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Chagas Disease / immunology
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Chemokine CCL2 / biosynthesis
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Chemokine CXCL1
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Chemokines / biosynthesis
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Chemokines, CXC*
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Chemotactic Factors / biosynthesis
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HeLa Cells
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Humans
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Inflammation Mediators / metabolism
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Intercellular Signaling Peptides and Proteins / biosynthesis
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Interleukin-8 / biosynthesis*
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Interleukin-8 / genetics
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Mucous Membrane / immunology
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Mucous Membrane / parasitology
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Nitric Oxide / biosynthesis*
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Trypanosoma cruzi / growth & development
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Trypanosoma cruzi / pathogenicity*
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Trypanosoma cruzi / physiology
Substances
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CXCL1 protein, human
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Chemokine CCL2
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Chemokine CXCL1
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Chemokines
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Chemokines, CXC
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Chemotactic Factors
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Inflammation Mediators
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Intercellular Signaling Peptides and Proteins
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Interleukin-8
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RNA, Messenger
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Nitric Oxide