Abstract:
:Enteropathogenic Escherichia coli (EPEC) interacts with intestinal epithelial cells, activating host signaling pathways leading to cytoskeletal rearrangements and ultimately diarrhea. In this study, we demonstrate that EPEC interacts with the macrophage-like cell line J774A.1 to inhibit phagocytosis by these cells. Antiphagocytic activity was also observed in cultured RAW macrophage-like cells upon EPEC infection. The EPEC antiphagocytic phenotype was dependent on the type III secretion pathway of EPEC and its secreted proteins, including EspA, EspB, and EspD. Intimin and Tir mutants displayed intermediate antiphagocytic activity, suggesting that intimate attachment mediated by intimin-Tir binding may also play a role in antiphagocytosis. Tyrosine dephosphorylation of several host proteins was observed following infection with secretion-competent EPEC but not with secretion-deficient mutants. Dephosphorylation was detectable 120 min after infection with EPEC, directly correlating with the onset of the antiphagocytic phenotype. Inhibition of protein tyrosine phosphatases by pervanadate treatment increased the number of intracellular wild-type EPEC organisms to levels seen with secretion-deficient mutants, suggesting that dephosphorylation events are linked to the antiphagocytic phenotype. No tyrosine phosphatase activity was detected with the EPEC-secreted proteins, suggesting that EPEC induces antiphagocytosis via a different mechanism than Yersinia species. Taken together, the present findings demonstrate a novel function for EPEC-secreted proteins in triggering macrophage protein tyrosine dephosphorylation and inhibition of phagocytosis.
journal_name
Infect Immunjournal_title
Infection and immunityauthors
Goosney DL,Celli J,Kenny B,Finlay BBdoi
10.1128/IAI.67.2.490-495.1999subject
Has Abstractpub_date
1999-02-01 00:00:00pages
490-5issue
2eissn
0019-9567issn
1098-5522journal_volume
67pub_type
杂志文章abstract::Botulinum C2 toxin has histopathological activity in the mouse intestine and induces fluid accumulation in intestinal loops. The toxin caused degenerative and necrotic changes in the intestinal mucosa: intracellular vacuolization of epithelial cells, desquamation and necrosis of the villous epithelium, intercellular e...
journal_title:Infection and immunity
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doi:10.1128/IAI.43.1.54-58.1984
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doi:10.1128/IAI.9.4.719-729.1974
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journal_title:Infection and immunity
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journal_title:Infection and immunity
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journal_title:Infection and immunity
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doi:10.1128/IAI.10.6.1292-1295.1974
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journal_title:Infection and immunity
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doi:10.1128/IAI.11.3.603-606.1975
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.66.12.5972-5979.1998
更新日期:1998-12-01 00:00:00
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journal_title:Infection and immunity
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.61.2.742-750.1993
更新日期:1993-02-01 00:00:00
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更新日期:2005-11-01 00:00:00
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journal_title:Infection and immunity
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更新日期:2002-02-01 00:00:00
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journal_title:Infection and immunity
pub_type: 杂志文章
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更新日期:2010-03-01 00:00:00
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journal_title:Infection and immunity
pub_type: 杂志文章
doi:10.1128/IAI.63.2.609-621.1995
更新日期:1995-02-01 00:00:00
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journal_title:Infection and immunity
pub_type: 杂志文章
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更新日期:1985-07-01 00:00:00