M cells--entryways of opportunity for enteropathogens.

Owen, Robert L.

doi:10.1084/jem.180.1.7

Cited by 45 publications

(22 citation statements)

References 13 publications

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“…The symptoms of untreated typhoid fever begin to resolve by the fourth week of infection, although relapse occurs in ≈ 10% of individuals apparently recovering from the infection (6). Intestinal complications can occur in the later stages of untreated infection; these include bleeding and perforation that are the result of an inflammatory response in the Peyer's patch, followed by necrosis and ulceration of the intestinal epithelium (7)(8)(9)(10). Intestinal perforation usually results in peritonitis and often requires surgical intervention.…”

Section: Typhoid Fevermentioning

confidence: 99%

SALMONELLOSIS: Host Immune Responses and Bacterial Virulence Determinants¹

Jones

Falkow

1996

Annu. Rev. Immunol.

368

273

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The lifestyle of bacterial pathogens requires them to establish infection in the face of host immunity. Upon entering a potential host, a variety of interactions are initiated, the outcome of which depends upon a myriad of attributes of each of the participants. In this review we discuss the interactions that occur between pathogenic Salmonella species and the host immune systems, but when appropriate to broaden perspective, we have provided a general overview of the interactions between bacterial pathogens and animal hosts. Pathogenic Salmonella species possess an array of invasion genes that produce proteins secreted by a specialized type III secretion apparatus. These proteins are used by the bacteria to penetrate the intestinal mucosa by invading and destroying specialized epithelial M cells of the Peyer's patches. This maneuver deposits the bacteria directly within the confines of the reticuloendothelial system. The host responds to these actions with nonspecific phagocytic cells and an inflammatory response as well as by activating specific cellular and humoral immune responses. Salmonella responds to this show of force directly. It appears that the bacteria invade and establish a niche within the very cells that have been sent to destroy them. Efforts are underway to characterize the factors that allow these intracellular bacteria to customize intracellular vacuoles for their own purposes. It is the constant play between these interactions that determines the outcome of the host infection, and clearly they will also shape the evolution of new survival strategies for both the bacterium and the host.

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Section: Typhoid Fevermentioning

confidence: 99%

SALMONELLOSIS: Host Immune Responses and Bacterial Virulence Determinants¹

Jones

Falkow

1996

Annu. Rev. Immunol.

368

273

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“…The identification of glycoconjugate expression and molecules unique to FAE and M-cell surfaces is now considered an attractive experimental model system to develop mucosal vaccines that can be targeted to Mcells so that penetration of the intestinal epithelium by infectious agents can be prevented Giannasca et al 1994;Owen 1994).…”

Section: Introductionmentioning

confidence: 99%

Lectin binding reveals divergent carbohydrate expression in human and mouse Peyer's patches

Sharma

Damme

Peumans

et al. 1996

Histochem Cell Biol

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The nature of cell-associated carbohydrates in the human intestine that may mediate transepithelial transport of bacterial and dietary lectins and their processing by the lymphoid cells of Peyer's patches is not known. Because the cell surface carbohydrate receptors for lectins may vary in different species, the glycoconjugates of human and mouse follicle-associated epithelium and gut-associated lymphoid tissue were compared. A panel of 27, mainly recently isolated, lectins were used to identify glycoconjugate expression in M-cells, enterocytes, goblet cells, lymphocytes and macrophages in mouse and human intestine. Mouse M-cells were exclusively labelled by fucose-specific lectins but in human follicle-associated epithelium no distinct M-cell staining pattern was observed. In the human Peyer's patches, Bryonia dioica lectin bound selectively to paracortical T-lymphocytes and Chelidonium majus lectin to germinal centre B-cells. Certain mannose-specific lectins (Galanthus nivalis, Hippeastrum hybrid) stained the tingible body macrophages in the germinal centre of human Peyer's patches but labelled the macrophages in the paracortical T-cell region of the mouse. The results indicate distinct differences in glycosylation between mouse and human Peyer's patches and their associated lymphoid cells. When considering cell surface glycoconjugates as target molecules for the gut immune system, care has to be taken to choose the appropriate lectin for each species.

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“…Despite these reports, there is a lack of direct evidence that human M cells are a major site of Salmonella invasion, although it is widely speculated that sites of Salmonella evasion in humans parallel mice and calf studies. Supporting this is the presence of ulcerations corresponding to the position of Peyer's patches in human typhoid (Owen, 1994).…”

Section: Cellsmentioning

confidence: 80%