Journal
JOURNAL OF INFECTIOUS DISEASES
Volume 184, Issue 6, Pages 743-753Publisher
UNIV CHICAGO PRESS
DOI: 10.1086/323035
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Funding
- NIAID NIH HHS [AI-24656] Funding Source: Medline
- NICHD NIH HHS [HD-12437, HD-31852] Funding Source: Medline
- NIDDK NIH HHS [DK-33506, DK-50989] Funding Source: Medline
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Shigella flexneri causes bacillary dysentery in humans by invading epithelial cells of the colon, which is characterized by an acute polymorphonuclear leukocyte (PMNL)-rich inflammation. Our recent studies demonstrated that cadaverine, a polyamine, specifically acts to abrogate transepithelial signaling to PMNL induced by S. flexneri. Here, insight is provided into the cellular mechanisms by which cadaverine attenuates the ability of Shigella species to induce PMNL signaling. It was found that cadaverine retards the lysis of the Shigella species-containing vacuole, suggesting that a blockade is established, in which the pathogen is prevented from adequately interacting with the cytoskeleton. Furthermore, an IcsA mutant of S. flexneri that cannot interact with the cytoskeleton and spreads intercellularly fails to induce transmigration of PMNL. Results indicate that cadaverine-induced compartmentalization of Shigella species to the phagolysosome might be a protective response of the host that directly contributes to the diminished ability of PMNL to transmigrate across model intestinal epithelia.
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