Intestinal epithelial cells infection

Particular strains of salmonellae (section 4.2) such as Sal. typhi, Sal. paratyphi and Sal. typhimurium are able not only to penetrate into intestinal epithelial cells and produce exotoxins but also to penetrate beyond into subepithelial tissues. These organisms therefore produce, in addition to the usual symptoms of salmonellosis, a characteristic systemic disease (typhoid and enteric fever). Following recovery frxm such infection the organism is commonly found associated with the gall bladder, hi this state, the recovered person will excrete the organism and form a reservoir for the infection of others. 

Shigella strains invade intestinal epithelial cells with subsequent multiplication, inflammation, and destruction.8 The organism infects the superficial layer of the gut, rarely penetrates beyond the mucosa, and seldom invades the bloodstream. However, bacteremia can occur in malnourished children and I immunocompromised patients. 

Artis, D., Potten, C.S., Else, K.J., Finkelman, F.D. and Grencis, R.K. (1999b) Trichuris muris. host intestinal epithelial cell hyperproliferation during chronic infection is regulated by interferon-y. Experimental Parasitology 92, 144-153. 

Although infection with C. parvum is considered predominantly secretory, histopathologic studies have revealed varying degrees of villous atrophy and infiltration of inflammatory cells beneath the epithelial mucosa [85, 86], Prostaglandins, which are known to induce cAMP-mediated apical chloride secretion and inhibit electroneutral sodium chloride and water absorption in enterocytes, have been demonstrated to be elevated in a porcine model of cryptosporidiosis [87], Inflammatory cytokines such as IL-1, IL-8 and TNF-a are induced in intestinal epithelial cell lines infected with Cryptosporidium and in animal models of cryptosporidiosis and have been postulated to play a role in pathogenesis [88, 89], Expression of TNF-a and IL-1 mRNA in the majority of jejunal biopsies of adult volunteers after experimental infection were also observed, although this did not correlate with the enteric symptoms [90]. 

Steiner TS, Lima AAM, Nataro JP, Guerrant RL Enteroaggregative Escherichia coli produce intestinal inflammation and growth impairment and cause interleukin-8 release from intestinal epithelial cells. J Infect Dis 1998 177 88-96. 

Langer RC, Riggs MW Cryptosporidium parvum apical complex glycoprotein CSL contains a sporozoite ligand for intestinal epithelial cells. Infect Immun 1999 67 5282-5291. 

Langer RC, Schaefer DA, Riggs MW Characterization of an intestinal epithelial cell receptor recognized by the Cryptosporidium parvum sporozoite ligand CSL. Infect Immun 2001 69 1661-1670. 

Laurent F, Eckmann L, Savidge TC, Morgan G, Theodos C, Naciri M, KagnoffMF Cryptosporidium parvum infection of human intestinal epithelial cells induces the polarized secretion of C-X-C chemokines. Infect Immun 1997 65 5067-5073. 

Firon, N., Ashkenazi, S., Mirelman, D., Ofek, I., and Sharon, N. (1987). Aromatic alpha-glycosides of mannose are powerful inhibitors of the adherence of type 1 Escherichia coli to yeast and intestinal epithelial cells. Infect. Immun. 55,474-476. 

Sukupolvi, S., Lorenz, R. G., Gordon, J. I., Bian, Z., Pfeifer, J. D., Normark, S. J., and Rhen, M. (1997). Expression of thin aggregative fimbriae promotes interaction of Salmonella typhi-murium SR-11 with mouse small intestinal epithelial cells. Infect. Immun. 65,5320-5325. 

Coccidia are intracellular protazoal parasites that are frequently found in the intestinal epithelial cells of animals they are also found in other tissues (liver), and are usually transmitted by faecal infection. The potential for infection is at its highest when young animals are brought together in intensive housing systems (e.g. poultry-broiler production). As a result coccidiosis is a major issue for the poultry industry throughout the world. 

Wehkamp, J., Harder, J., Wehkamp, K., Wehkamp-von Meissner, B., Schlee, M., Enders, C., Sonnenborn, U., Nuding, S., Bengmark, S., Fellermann, K., Schroder, J. M., and Stange, E. F. (2004). NF-kB- and AP-l-mediated induction of human p-defensin-2 in intestinal epithelial cells by Escherichia coli Nissle 1917 A novel effect of a probiotic bacterium. Infect. Immun. 72(10), 5750-5758. 

Fig. 5.1 Pathogenesis of Salmonella Typhimurium and Salmonella Typhi. Upon ingestion, Salmonella travel to the small intestine. The bacteria invade Microfold (M) cells and other intestinal epithelial cells through the apical surface to cause infection. (A). Salmonella Typhimurium remains localized in the small intestine and induces an inflammatory host immune response, resulting in bacterial clearance from immunocompetent individuals. (B). Salmonella Typhi escapes from intestinal epithelial cells at the basolateral surface of the intestinal epithelium, enters phagocytes, and evades the host innate immune response, resulting in systemic infection...

Kanipes, M.I., Holder, L.C., Corcoran, A.T., Moran, A.P., Guerry, P. A deep-rough mutant of Campylobacter jejuni 81-176 is non-invasive for intestinal epithelial cells. Infect Immun 72 (2004) 2452-2455. 

Intestinal mucosal cells also can activate mediators of inflammation. Intestinal epithelial cells express an array of cytokine receptors and produce a spectrum of immune mediators, suggesting that they play an integral role in mucosal innate and acquired immunity (Dwinell et al 1999). Consistent with those functions, human intestinal epithelial cells have been shown to upregu-late the expression and secretion of a variety of proinflammatory chemokines in response to infection with enteroinvasive pathogens or stimulation with proinflammatory cytokines. Epithelial cell-derived chemokines appear to act as mediators of intercellular communication between the epithelium and immune and inflammatory cells in the adjacent and underlying mucosa. 

Gagliardo LF, McVay CS, Appleton JA (2002) Molting, ecdysis, and reproduction of Trichinella spiralis are supported in vitro by intestinal epithelial cells. Infect Immun 70 1853-1859 Gelletlie R, Stuart J, Soltanpoor N, Armstrong R, Nichols G (1997) Cryptosporidiosis associated with school milk. Lancet 350 1005-1006... 

Some bacterial toxins contain a subunit that penetrates the plasma membrane of cells and catalyzes a chemical modification of Gscj-GTP that prevents hydrolysis of bound GTP to GDP. As a result, remains in the active state, continuously activating adenylyl cyclase in the absence of hormonal stimulation. Cholera toxin produced by the bacterium Vibrio cholera and enterotoxlns produced by certain strains of E. coll act in this way on intestinal epithelial cells. The resulting excessive rise in Intracellular cAMP leads to the loss of electrolytes and water into the intestinal lumen, producing the watery diarrhea characteristic of infection by these bacteria. 

Most of the current knowledge on the biological contributions of the two COX isoforms has come from studies by NSAID inhibition, COX-2 induction or both. Both gene disruption and overexpression of the COX isoforms have recently been developed as alternative approaches to investigate the problem. It has been demonstrated that COX-1 gene disruption reduces arachidonic acid-induced inflammation and indomethacin-induced gastric ulceration in mice [25]. On the other hand, renal abnormalities and an altered inflammatory response were observed in mice with COX-2 gene disruption [26,27], Rat intestinal epithelial cells permanently infected with a COX-2 expression vector showed not only the elevated expression level of COX-2 protein, but also both increased adhesion to extracellular matrix and inhibition of apoptosis [28]. 

The apparent ease with which cholera vibrios migrate through the intestinal mucus suggests that there is little permanent adhesion of the bacterium to this layer. Microscopical examination of cholera-infected rabbit intestine reveals large numbers of vibrios attached to the brush border surfaces of intestinal epithelial cells, but no evidence of fimbriae can be seen. There appear to be at least two highly specific receptors for the cholera vibrio on the mucosal surface, one of which is fucose-sensitive and located on the brush border epithelium. The location of the second fucose-resistant binding site is unclear. V. cholerae, like many other vibrios, produce a protein-rich slime capsule. There is no evidence that this layer has any adhesive properties, indeed the reverse may be true, since slime production and haemagglutinating activities are inversely related. 

Joe A, Verdon R, Tzipori S, Keusch GT, Ward HD (1998) Attachment of Cryptosporidium parvum sporozoites to human intestinal epithelial cells. Infect Immun 66 3429-32. 

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