Mesenteric Lymph Nodes Confine Dendritic Cell-Mediated Dissemination of<i>Salmonella enterica</i>Serovar Typhimurium and Limit Systemic Disease in Mice

Voedisch, Sabrina; Koenecke, Christian; David, Sascha; Herbrand, Heike; Förster, Reinhold; Rhen, Mikael; Pabst, Oliver

doi:10.1128/iai.00272-09

Cited by 102 publications

(114 citation statements)

References 38 publications

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“…Indeed, precedence for the importance of luminal spread and a pool of replicating pathogens in the intestinal mucosa has been established in models of L. monocytogenes, Salmonella enterica, and Yersinia pseudotuberculosis infection (47)(48)(49). Melton-Witt et al proposed that luminal shedding acts as a mechanism for bacterial spread and further dissemination after showing that L. monocytogenes shed from villi into the lumen can infect Peyer's patches (47).…”

Section: Discussionmentioning

confidence: 99%

Replication and Distribution of Toxoplasma gondii in the Small Intestine after Oral Infection with Tissue Cysts

Gregg¹,

Taylor

John

et al. 2013

Infect Immun

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Natural infection by Toxoplasma gondii occurs via oral ingestion of tissue cysts that rupture in the small intestine, releasing zoites that infect locally before disseminating throughout the host. The studies presented here used fluorescent parasites combined with flow cytometry and multiphoton microscopy techniques to understand the events associated with parasite replication in the mucosa. At 3 days postinfection with tissue cysts, parasites were localized in small foci and flow cytometry revealed parasites present in macrophages, neutrophils, and monocytes in the lamina propria. By day 6 postinfection, there were large foci of replicating parasites; however, foci unexpectedly varied in the number of villi involved and were associated with the presence of viable tachyzoites within the intestinal lumen. Consistent with the flow cytometry data, neutrophils and monocytes in the lamina propria were preferentially associated with parasite plaques. In contrast, dendritic cells comprised a small fraction of the infected immune cell population and were localized at the periphery of parasite plaques. Together, these findings reveal the formation of localized sites of parasite replication and inflammation early during infection and suggest that sustained replication of T. gondii in the gut may be a function of pathogen luminal spread.

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Section: Discussionmentioning

confidence: 99%

Replication and Distribution of Toxoplasma gondii in the Small Intestine after Oral Infection with Tissue Cysts

Gregg¹,

Taylor

John

et al. 2013

Infect Immun

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“…Thus, the yopK mutant reached the MLN that constitute the critical barrier for preventing systemic infection by both commensals and pathogens (42,43) but failed to disseminate further. Analysis of initial colonization of the different intestinal organs using IVIS and immunofluorescence staining showed that Y. pseudotuberculosis lacking YopK colonized PPs and MLN more rapidly than the wild-type strain.…”

Section: Discussionmentioning

confidence: 99%

Role of YopK in Yersinia pseudotuberculosis Resistance against Polymorphonuclear Leukocyte Defense

et al. 2013

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The enteropathogen Yersinia pseudotuberculosis can survive in the harsh environment of lymphoid compartments that abounds in immune cells. This capacity is dependent on the plasmid-encoded Yersinia outer proteins (Yops) that are delivered into the host cell via a mechanism involving the Yersinia type III secretion system. We show that the virulence protein YopK has a role in the mechanism by which Y. pseudotuberculosis avoids the polymorphonuclear leukocyte or neutrophil (PMN) defense. A yopK mutant, which is attenuated in the mouse infection model, where it fails to cause systemic infection, was found to colonize Peyer's patches and mesenteric lymph nodes more rapidly than the wild-type strain. Further, in mice lacking PMNs, the yopK mutant caused full disease with systemic spread and typical symptoms. Analyses of effects on PMNs revealed that both the wild-type strain and the yopK mutant inhibited internalization and reactive oxygen species production, as well as neutrophil extracellular trap formation by PMNs. However, the wild-type strain effectively avoided induction of PMN death, whereas the mutant caused a necrosis-like PMN death. Taken together, our results indicate that YopK is required for the ability of Yersinia to resist the PMN defense, which is critical for the virulence of the pathogen. We suggest a mechanism whereby YopK functions to prevent unintended Yop delivery and thereby PMN disruption, resulting in necrosis-like cell death, which would enhance the inflammatory response favoring the host.

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“…Surgery was performed as previously described (40). Briefly, the small intestine and cecum, together with MLN, were exteriorized through a 1-cm-wide incision along the abdomen and kept humid with PBS.…”

Section: Methodsmentioning

confidence: 99%

Retinoic acid induces homing of protective T and B cells to the gut after subcutaneous immunization in mice

Hammerschmidt¹,

Friedrichsen²,

Boelter³

et al. 2011

J. Clin. Invest.

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139

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Mesenteric Lymph Nodes Confine Dendritic Cell-Mediated Dissemination ofSalmonella entericaSerovar Typhimurium and Limit Systemic Disease in Mice

Cited by 102 publications

References 38 publications

Replication and Distribution of Toxoplasma gondii in the Small Intestine after Oral Infection with Tissue Cysts

Replication and Distribution of Toxoplasma gondii in the Small Intestine after Oral Infection with Tissue Cysts

Role of YopK in Yersinia pseudotuberculosis Resistance against Polymorphonuclear Leukocyte Defense

Retinoic acid induces homing of protective T and B cells to the gut after subcutaneous immunization in mice

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