Apoptosis and Gastrointestinal Disease

Palejwala, Altaf; Watson, Alastair

doi:10.1097/00005176-200010000-00004

Cited by 6 publications

(6 citation statements)

References 74 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As we did not study the extrinsic apoptotic pathway in this study, an additive role of the extrinsic pathway could not be ruled out for our patients. However, keeping in mind the results of the previously published studies, [8][9][10][11][12][13][14] we can conclude that, along with the extrinsic pathway, the common as well as the intrinsic apoptotic pathways are active in treatment-naïve patients with celiac disease.…”

Section: Commentmentioning

confidence: 70%

“…[1][2][3][4][5] While a few studies have suggested a role for apoptosis in villous atrophy in patients with celiac disease, others do not confirm this finding. [6][7][8][9][10][11][12][13][14] In such a study, Moss et al 6 had reported presence of fragmented DNA in the intestinal mucosa of treatment-naïve patients with celiac disease, which disappeared after administration of gluten-free diet. Most other studies in this respect were limited to the identification of the role of FAS and FAS-Lmediated apoptosis.…”

mentioning

confidence: 99%

“…Most other studies in this respect were limited to the identification of the role of FAS and FAS-Lmediated apoptosis. [10][11][12][13][14] (2005) have identified the role of extrinsic apoptotic pathway activation in the mucosa of patients with celiac disease. On the other hand, apoptosis can be induced either by the extrinsic or the intrinsic apoptotic pathways.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Mechanism of Villous Atrophy in Celiac Disease: Role of Apoptosis and Epithelial Regeneration

Shalimar

Das

Sreenivas

et al. 2013

Archives of Pathology &Amp; Laboratory Medicine

View full text Add to dashboard Cite

Context.—The data on status of apoptosis in patients with celiac disease are conflicting. Furthermore, complex interaction between intrinsic and common apoptotic pathways, apoptotic inhibitors, and epithelial cell proliferation is largely unclear for patients with celiac disease. Objectives.—To determine the role of apoptosis and epithelial cell regeneration in celiac disease. Design.—Twenty-five treatment-naïve patients with celiac disease and 6 patients with functional dyspepsia, as controls, were included and duodenal biopsy specimens from all were subjected to immunohistochemistry with markers of intrinsic apoptotic pathway (AIF, H2AX, p53), common pathway (CC3, M30), apoptotic inhibitors (XIAP, Bcl2), and epithelial proliferation (Ki-67). Apoptotic and proliferation indices were calculated. Results.—Expression of end-apoptotic products, that is, H2AX in the cell nuclei (P = .01) and M30 in the cell cytoplasm (P < .01), was significantly upregulated in celiac disease in comparison to controls. Cleaved caspase-3 was also upregulated in villous cytoplasm in celiac disease. Apoptotic inhibitor Bcl2 was significantly down-regulated in celiac disease in comparison to controls. In addition, Ki-67 proliferation index was upregulated both in the crypts and villous mucosal epithelium in comparison to the crypts of the controls. Conclusions.—Treatment-naïve patients with celiac disease have significantly higher level of apoptosis that involves both the common and intrinsic apoptotic pathways. Increased apoptosis and unequaled cell regeneration in crypts probably results in villous atrophy. Down-regulation of apoptotic inhibitors in treatment-naïve celiac disease imparts an additional pro-apoptotic effect.

show abstract

Section: Commentmentioning

confidence: 70%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Mechanism of Villous Atrophy in Celiac Disease: Role of Apoptosis and Epithelial Regeneration

Shalimar

Das

Sreenivas

et al. 2013

Archives of Pathology &Amp; Laboratory Medicine

View full text Add to dashboard Cite

show abstract

“…IEC homeostasis is maintained in the gastrointestinal tract mainly via proliferative activity and apoptosis [6]; cells shed naturally are rapidly replenished by stem cells in villi crypts, every 3-5 days on average [7]. Due to this large degree of cell turnover and the physiological requirement for apoptotic cell death, it follows that dysregulated apoptosis is indicated in a number of gastrointestinal diseases [6,[8][9][10][11]. Since a reduction in disproportionate apoptosis improves intestinal health [12], it is worthwhile to further delineate the nature of this physiological process.…”

Section: Introductionmentioning

confidence: 99%

Lactobacillus plantarum 299v Prevents Caspase-Dependent Apoptosis In Vitro

Dykstra

Hyde

Mackenzie

et al. 2011

Probiotics & Antimicro. Prot.

View full text Add to dashboard Cite

Selective microbes used as probiotics can enhance epithelial cell protection. We have previously shown that a Lactobacillus plantarum strain 299v (Lp299v) has the ability to induce mucin genes. In the current study, we utilized a cytokine model of inflammation in cell culture to study the modulation of apoptosis by this probiotic. HT-29 cells were pre-incubated with the Lp299v or L. plantarum strain adh- (Lpadh-), a non-adherent derivative of Lp299v. Cells were challenged with a mixture of cytokines (TNF-α, IFN-γ, and IL-1a) to imitate conditions of inflammation. To assess for cell death, we evaluated TUNEL, multi-caspase, and caspase-3 and caspase-7 activity assays. There was a marked decrease in apoptosis as measured by TUNEL(+) cells in samples pre-treated with Lp299v (18.7 ± 4.1%, p < 0.01) and Lpadh- (16.6 ± 3.2%, p < 0.05) prior to cytokine exposure when compared to cells (43.6 ± 6.2%) exposed to the cytokine mixture. Lp299v pre-incubation with HT-29 cells reduced caspase(+) cells in the multi-caspase activity assay (3.6 ± 0.6%, p < 0.05) compared to cells exposed to cytokines (68.9 ± 5.1%) whereas Lpadh- did not (46.8 ± 17.5%, p > 0.05). Similarly, caspase-3, caspase-7 activity was also reduced by Lp299v. Selected probiotics may confer an exogenous protective effect at the mucosal-luminal interface for intestinal epithelial cells via alteration of caspase-dependent apoptotic pathways.

show abstract

“…15 Apoptosis plays an essential role in the normal physiologic turnover and renewal of cells, with the elimination of senescent cells and the maintenance of the appropriate cell number and function in actively proliferating GI mucosa. 33…”

mentioning

confidence: 99%

Gut Immunology and the Differential Response to Feeding and Starvation

et al. 2003

View full text Add to dashboard Cite

Animal and human research has established the beneficial effects of enteral nutrition on the gut. Both the innate and acquired immune systems are bolstered by enteral alimentation. Emerging clinical concepts tie these beneficial effects to a significant influence on the host immune response to stressors during critical illness. In this article, we examine how enteral nutrition impacts gastrointestinal immunity and demonstrate how these changes may affect the body's systemic immune response to nongastrointestinal challenges. This modulatory effect occurs because of changes in the pattern of cytokine secretion and alterations in lymphocyte and neutrophil recruitment. Imbalances in these regulatory mechanisms may be the engine driving hyperresponsiveness to subsequent challenges in the critically ill patient.

show abstract

Apoptosis and Gastrointestinal Disease

Cited by 6 publications

References 74 publications

Mechanism of Villous Atrophy in Celiac Disease: Role of Apoptosis and Epithelial Regeneration

Mechanism of Villous Atrophy in Celiac Disease: Role of Apoptosis and Epithelial Regeneration

Lactobacillus plantarum 299v Prevents Caspase-Dependent Apoptosis In Vitro

Gut Immunology and the Differential Response to Feeding and Starvation

Contact Info

Product

Resources

About