The Mucosal Phase of Listeria Infection

Havell, Edward A.; Beretich, Guy R.; Carter, Philip B.

doi:10.1016/s0171-2985(99)80056-4

Cited by 26 publications

(21 citation statements)

References 35 publications

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“…administration (Table 3) (Table 3). M cells in the PP have been implicated in the mechanism of murine listeriosis [32], although this issue remains controversial [33]. Since conventional TNF-KO mice develop normal M cells in their PP [30] while TNF D/D mice lack PP altogether, our results clearly establish that PP in TNF -/-mice per se play no obligatory role in pathogenesis or protection of mice from intestinal Listeria infection.…”

Section: Since Tnfmentioning

confidence: 60%

Novel tumor necrosis factor‐knockout mice that lack Peyer's patches

et al. 2005

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We generated a novel tumor necrosis factor (TNF) null mutation using Cre-loxP technology. Mice homozygous for this mutation differ from their "conventional" counterparts; in particular, they completely lack Peyer's patches (PP) but retain all lymph nodes. Our analysis of these novel TNF-knockout mice supports the previously disputed notion of the involvement of TNF-TNFR1 signaling in PP organogenesis. Availability of TNF-knockout strains both with and without PP enables more definitive studies concerning the roles of TNF and PP in various immune functions and disease conditions. Here, we report that systemic ablation of TNF, but not the presence of PP per se, is critical for protection against intestinal Listeria infection in mice.

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Section: Since Tnfmentioning

confidence: 60%

Novel tumor necrosis factor‐knockout mice that lack Peyer's patches

et al. 2005

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“…Translocation of L. monocytogenes across the FAE and its underlying lymphoid follicles, or across the colonic mucosal barrier via an as yet undefined InlA-Ecad-independent pathway, provides potential alternate routes for bacterial translocation across the gut barrier (31,32). Our preliminary experiments in conventionally raised adult Lt␤R(Ϫ/Ϫ) mice that lack Peyer's patches (33) suggest that these animals are resistant to intestinal invasion by WT L. monocytogenes.…”

Section: Inla Is Not the Major Bacterial Determinant Of L Monocytogementioning

confidence: 86%

Functional Genomic Studies of the Intestinal Response to a Foodborne Enteropathogen in a Humanized Gnotobiotic Mouse Model

Lecuit

Sonnenburg

Cossart

et al. 2007

Journal of Biological Chemistry

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Members of the genus Listeria provide a model for defining host responses to invasive foodborne enteropathogens. Active translocation of Listeria monocytogenes across the gut epithelial barrier is mediated by interaction of bacterial internalin (InlA) and its species-specific host receptor, E-cadherin, whereas translocation across Peyer's patches through M-cells is InlAindependent. To define microbial determinants and molecular correlates of the host response to translocation via these two routes, we colonized germ-free transgenic mice expressing the human enterocyte-associated E-cadherin receptor with wildtype (WT) or mutant L. monocytogenes strains, or its nonpathogenic noninvasive relative Listeria innocua, or with Bacteroides thetaiotaomicron, a prominent gut symbiont. Mouse GeneChips, combined with Ingenuity Pathway software, were used to identify canonical signaling pathways that comprise the response to WT L. monocytogenes versus the other species. Gain-and loss-of-function experiments with L. innocua and L. monocytogenes, respectively, demonstrated that the 773-member transcriptional signature of the response to WT L. monocytogenes is largely conserved in the ⌬inlA mutant. Internalin-dependent responses include down-regulation of gene networks involved in various aspects of lipid, amino acid, and energy metabolism and up-regulation of immunoinflammatory responses. The host response is markedly attenuated in a listeriolysin-deficient (⌬hly) mutant despite its ability to be translocated to the lamina propria. Together, these studies establish that hly, rather than bacterial invasion of the lamina propria mediated by InlA, is a dominant determinant of the intensity of the host response to L. monocytogenes infection via the oral route.

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“…route and have focused on the immune responses in the spleen. The mucosal T cell response to enteric infection with L. monocytogenes is largely undefined (20).…”

mentioning

confidence: 99%

Intestinal and Splenic T Cell Responses to EntericListeria monocytogenesInfection: Distinct Repertoires of Responding CD8 T Lymphocytes

Huleatt

Pilip

Kerksiek

et al. 2001

The Journal of Immunology

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Listeria monocytogenes is an intracellular bacterium that causes systemic infections after traversing the intestinal mucosa. Clearance of infection and long term protective immunity are mediated by L. monocytogenes-specific CD8 T lymphocytes. In this report, we characterize the murine CD8 T cell response in the lamina propria and intestinal epithelium after enteric L. monocytogenes infection. We find that the frequency of MHC class Ia-restricted, L. monocytogenes-specific T cells is ∼4- to 5-fold greater in the lamina propria than in the spleen of mice after oral or i.v. infection. Although the kinetics of T cell expansion and contraction are similar in spleen, lamina propria, and intestinal epithelium, high frequencies of Ag-specific T cells are detected only in the lamina propria 1 mo after infection. In contrast to MHC class Ia-restricted T cells, the frequency of H2-M3-restricted, L. monocytogenes-specific T cells is decreased in the intestinal mucosa relative to that found in the spleen. In addition to this disparity, we find that MHC class Ia-restricted CD8 T cells specific for a dominant L. monocytogenes epitope have different TCR Vβ repertoires in the spleen and intestinal mucosa of individual mice. These findings indicate that the intestinal mucosa is a depot where L. monocytogenes-specific effector CD8 T cells accumulate during and after infection irrespective of immunization route. Furthermore, our results demonstrate that CD8 T cell populations in these two sites, although overlapping in Ag specificity, are distinct in terms of their repertoire.

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The Mucosal Phase of Listeria Infection

Cited by 26 publications

References 35 publications

Novel tumor necrosis factor‐knockout mice that lack Peyer's patches

Novel tumor necrosis factor‐knockout mice that lack Peyer's patches

Functional Genomic Studies of the Intestinal Response to a Foodborne Enteropathogen in a Humanized Gnotobiotic Mouse Model

Intestinal and Splenic T Cell Responses to EntericListeria monocytogenesInfection: Distinct Repertoires of Responding CD8 T Lymphocytes

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