A recombinant Salmonella typhimurium vaccine strain is taken up and survives within murine Peyer's patch dendritic cells

Hopkins,; Niedergang, Florence; Corthesy-Theulaz,; Kraehenbuhl,

doi:10.1046/j.1462-5822.2000.00035.x

Cited by 149 publications

(121 citation statements)

References 45 publications

Supporting

Mentioning

116

Contrasting

Order By: Relevance

“…In addition, ex vivo ileal loop assays demonstrate that Salmonella infect Peyer's patch dendritic cells (38). It was also shown recently that Salmonella can cross the intestinal barrier within CD18-expressing phagocytes (39,40), which include dendritic cells.…”

Section: Discussionmentioning

confidence: 96%

“…An important role for dendritic cells in engaging T lymphocytes during Salmonella infection is suggested by in vitro evidence that these professional phagocytes efficiently present Salmonella-derived Ags to both CD4 ϩ and CD8 ϩ T cells either directly or following ingestion of infected macrophages that have undergone Salmonella-induced death (57,58). Ex vivo data showing that Salmonella reside within Peyer's patch dendritic cells (38) and in vivo evidence demonstrating that flagellin-specific CD4 ϩ T cells, in response to Salmonella ingestion, rapidly migrate to and expand within the gutassociated lymphoid tissue (59) further suggest that resident dendritic cells may stimulate T lymphocyes during natural infection. To better understand these intricate interactions, we are currently investigating how Salmonella-induced macrophage and dendritic cell death affects the ability of an infected host to mount a protective immune response against this frequently lethal pathogen.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Salmonella Rapidly Kill Dendritic Cells via a Caspase-1- Dependent Mechanism

Velden

Velasquez

Starnbach

2003

The Journal of Immunology

110

View full text Add to dashboard Cite

Dendritic cells provide a critical link between innate and acquired immunity. In this study, we demonstrate that the bacterial pathogen Salmonella enterica serovar Typhimurium can efficiently kill these professional phagocytes via a mechanism that is dependent on sipB and the Salmonella pathogenicity island 1-encoded type III protein secretion system. Rapid phosphatidylserine redistribution, caspase activation, and loss of plasma membrane integrity were characteristic of dendritic cells infected with wild-type Salmonella, but not sipB mutant bacteria. Caspase-1 was particularly important in this process because Salmonella-induced dendritic cell death was dramatically reduced in the presence of a caspase-1-specific inhibitor. Furthermore, dendritic cells obtained from caspase-1-deficient mice, but not heterozygous littermate control mice, were resistant to Salmonella-induced cytotoxicity. We hypothesize that Salmonella have evolved the ability to selectively kill professional APCs to combat, exploit, or evade immune defense mechanisms.

show abstract

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Salmonella Rapidly Kill Dendritic Cells via a Caspase-1- Dependent Mechanism

Velden

Velasquez

Starnbach

2003

The Journal of Immunology

110

View full text Add to dashboard Cite

show abstract

“…S. typhimurium PhoPc strain transformed with the pKKGFP plasmid was kindly provided by F. Niedergang (24,25). Further, GFP-expressing Yersinia pseudotuberculosis, Escherichia coli-invasin, and E. coli were prepared by the method described (26,27).…”

Section: Cell Stainingmentioning

confidence: 99%

Intestinal villous M cells: An antigen entry site in the mucosal epithelium

Jang

Kweon

Iwatani

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

418

331

View full text Add to dashboard Cite

T he huge intestinal surface area is physically protected by a layer of tightly joined epithelial cells, which prevent most enteric environmental antigens from penetrating the host (1). However, entry into the host is made possible by a special gateway, comprised of M cells, located over organized mucosal lymphoid follicles such as Peyer's patches (PP). The M cells, characterized by an irregular brush border and reduced glycocalyx, efficiently take up and transport a wide variety of macromolecules and microorganisms from the gut lumen to the inside of the PP (2-6), which contain all of the necessary lymphoid cells for the induction and regulation of antigen-specific IgA responses (7). However, the origin of M cells and the regulation of their development are not understood. A previous study (8) The common mucosal immune system (CMIS), which connects the inductive (e.g., PP) and effector (e.g., lamina propria; LP) sites, has been shown to be a central pathway for the induction of antigen-specific IgA immune responses in the gastrointestinal tract (7). For example, oral administration of Salmonella typhimurium leads to the transport of the bacterial antigen from the lumen of the intestinal tract into the PP by means of M cells for the initial priming of antigen-specific CD4 ϩ T cells and IgA-committed B cells (12). These antigen-sensitized cells leave the PP and contribute to the subsequent induction of Salmonella-specific IgA response in the distant intestinal LP by means of CMIS. In addition to the wellcharacterized CMIS-dependent IgA induction pathway, recent evidence suggests the presence of an additional IgA induction pathway that is independently operated from the PP-originated CMIS (13-15). Interestingly, it also has been reported that induction of intestinal mucosal IgA against the commensal bacteria was independent from T cell help and organized lymphoid tissue (16). Further, our recent study (17) has demonstrated that antigenspecific IgA antibody responses can be induced in the absence of PP. These studies imply the existence of a PP-independent mucosal immune pathway for dietary antigen and bacteria uptake.A recent study (18) has suggested that the invasion gene (SPI1)-deficient S. typhimurium can be disseminated from the intestinal epithelium to the systemic compartment in the absence of PPassociated M cells by means of the CD18-dependent pathway. Further, dendritic cells in the lamina propria of the small intestine expressing tight junction protein offer another possible antigen uptake site (19). Thus, intestinal DCs are capable of extending dendrites to the lumen side by opening the tight junction. However, the exact mechanism for inducing Ag-specific immune responses independently of PP requires further elucidation.In this study, we have discovered intestinal villous M cells, which serve as an antigen gateway for the sampling of gut bacteria and subsequent induction of Ag-specific immune responses in a PPindependent manner. These lines of study are crucial for understanding the mechanisms of antige...

show abstract

“…The effector and memory T cells that populate the intestine are reported to be produced in PPs and mesenteric lymph nodes (MLNs) (6,11,12). In PPs, M cells in the epithelium transport luminal Ags to the apical side (13), where dendritic cells wait for them (14)(15)(16). These dendritic cells prime and activate T N cells that enter the PP and induce the expression of a 4 b 7 , a gut-homing receptor, on the T cells (17).…”

mentioning

confidence: 99%

Homeostatic Proliferation of Naive CD4+ T Cells in Mesenteric Lymph Nodes Generates Gut-Tropic Th17 Cells

Kawabe

Sun

Fujita

et al. 2013

The Journal of Immunology

View full text Add to dashboard Cite

Homeostatic proliferation of naive T cells in the spleen and cutaneous lymph nodes supplies memory–phenotype T cells. The “systemic” proliferative responses divide distinctly into fast or slow cell division rates. The fast proliferation is critical for generation of effector memory T cells. Because effector memory T cells are abundant in the lamina propria of the intestinal tissue, “gut-specific” homeostatic proliferation of naive T cells may be important for generation of intestinal effector memory T cells. However, such organ-specific homeostatic proliferation of naive T cells has not yet been addressed. In this study, we examined the gut-specific homeostatic proliferation by transferring CFSE-labeled naive CD4+ T cells into sublethally irradiated mice and separately evaluating donor cell division and differentiation in the intestine, mesenteric lymph nodes (MLNs), and other lymphoid organs. We found that the fast-proliferating cell population in the intestine and MLNs had a gut-tropic α4β7+ Th17 phenotype and that their production was dependent on the presence of commensal bacteria and OX40 costimulation. Mesenteric lymphadenectomy significantly reduced the Th17 cell population in the host intestine. Furthermore, FTY720 treatment induced the accumulation of α4β7+IL-17A+ fast-dividing cells in MLNs and eliminated donor cells in the intestine, suggesting that MLNs rather than intestinal tissues are essential for generating intestinal Th17 cells. These results reveal that MLNs play a central role in inducing gut-tropic Th17 cells and in maintaining CD4+ T cell homeostasis in the small intestine.

show abstract

A recombinant Salmonella typhimurium vaccine strain is taken up and survives within murine Peyer's patch dendritic cells

Cited by 149 publications

References 45 publications

Salmonella Rapidly Kill Dendritic Cells via a Caspase-1- Dependent Mechanism

Salmonella Rapidly Kill Dendritic Cells via a Caspase-1- Dependent Mechanism

Intestinal villous M cells: An antigen entry site in the mucosal epithelium

Homeostatic Proliferation of Naive CD4+ T Cells in Mesenteric Lymph Nodes Generates Gut-Tropic Th17 Cells

Contact Info

Product

Resources

About