Enterocytes apoptosis

T cell and cytokine regulation of enterocyte apoptosis may also be important in the expulsion of nematodes, in particular T. spiralis and T. muris, which inhabit an intracellular niche. Certainly an increase in the number of apoptotic cells within the epithelium is observed around the period of expulsion of T. muris in resistant mouse strains (D. Artis, C.S. Potten and R.K. Grencis, unpublished). Apoptosis of host enterocytes may dislodge the nematode or perhaps expose vital feeding organs to immune attack, and so enhance expulsion. Whether enterocyte apoptosis results from the burrowing action of the worms or a tissue repair mechanism, or is involved in expulsion, remains to be investigated. 

Piguet, P.F., Vesin, C., Guo, J., Donati, Y. and Barazzone, C. (1998) TNF-induced enterocyte apoptosis in mice is mediated by the TNF receptor 1 and does not require p53. European Journal of Immunology 28, 3499-3505. 

In vivo studies using mouse models have proved that curcumin modifies apoptosis resistance, leading to the inhibition of tumor formation and the prevention of adenoma development in the intestinal tract. The chemopreven-tive effect of curcumin for intestinal tumors in Min/+ mice was investigated. A dietary level of 0.15% curcumin decreased tumor formation in Min—/— mice by 63%. Examination of intestinal tissue from the treated animals showed the tumor prevention by curcumin was associated with increased enterocyte apoptosis and proliferation. Curcumin also decreased expression of the oncoprotein (S-catenin in the erythrocytes of the Min/+ mouse, an observation previously associated with an antitumor effect. Curcumin enhanced PhlP-induced apoptosis and inhibited PhIP-induced tumorigenesis in the proximal small intestine of Ape (min) mice. Experiments performed on intestinal tumors in C57BL/6J-Min/+ (Min/+) mice demonstrated that curcumin has a regulatory role in lymphocyte-mediated immune function [Churchill et al., 2000]. Furthermore, levels of COX-2 protein expression have been found to reflect the retardation of adenoma development in mouse intestines after treatment with curcumin [Tunstall et al., 2006]. 

Di Sabatino, A., R. Ciccocioppo, O. Luinetti, L. Ricevuti, R. Morera, M.G. Cifone, E. Solcia, and G.R. Corazza. Increased Enterocyte Apoptosis in Inflamed Areas of Crohn s... 

Coopersmith, C. M. and Gordon, J. I. (1997) Gamma-ray-induced apoptosis in transgenic mice with proliferative abnormalities in their intestinal epithelium re-entry of villus enterocytes into the cell cycle does not affect their radioresistance but enhances the radiosensitivity of the crypt by inducing p53. Oncogene 15,131-141. 

Glaeser et al. have shown that the majority of shed human enterocytes collected from an intestinal perfusion were still functionally active and did not show signs of apoptosis [38]. On the basis of a validation of the Loc-I-Gut system for the study of... 

Goh J, Baird AW, O Keane C, Watson RW, Cottell D, Bernasconi G, Petasis NA, Godson C, Brady HR, MacMathuna P (2001) Lipoxin A(4) and aspirin-triggered 15-epi-lipoxin A(4) antagonize TNF-alpha-stimulated neutrophil-enterocyte interactions in vitro and attenuate TNF-alpha-induced chemokine release and colonocyte apoptosis in human intestinal mucosa ex vivo. J Immunol 167 2772-2780... 

Since APC mutations have been described in RER+ tumors (Huang et al., 1996) and since APC mutations are initiating mutations in the evolution of common CRCs, we describe the model for the case in which loss of APC is the initiating event of variant cancer. It is proposed that loss of APC function in an RER+ enterocyte can simultaneously have two consequences (1) Block apoptosis, thus allowing the continuation of the mutation-driven process (2) lead to adenoma formation, thus initiating the selection-driven... 

The majority of shed enterocytes collected during the perfusion are still functionally active and show no signs of apoptosis [67, 68]. On that basis, Petri et al. [19] were able to study the cellular response to phytochemicals In human enterocytes In vivo, by measuring differences in mRNA levels of phase 2 metabolizing enzymes. Indeed, the authors observed an immediate cellular response of the enterocytes to phytochemicals present in a crude vegetable extract [19]. 

Initial reports on PTXs hepatotoxicity prompted the study of in vitro effects of these toxins on hepatocytes. There are several reports on PTX-1 and -2 in vitro cytotoxicity to hepatocytes. PTX-1 has been demonstrated to induce morphological changes and apoptosis in freshly prepared rat and sahnon hepatocytes [31,32]. PTX-1 toxic effects on primary cultures of liver cells have also been reported as disarrangement of actin and microtubule cytoskeleton [33]. Recently, in our laboratory, we found that actin cytoskeleton of primary rat hepatocytes was also altered by PTX-2 and -11 in the same way as PTX-1 but with a slightly higher potency [34]. Another primary cell type sensitive to PTXs is fresh enterocytes isolated from rabbit, in which PTX-6 induces a significant depolimeriza-tion of actin filaments [35]. 

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