Cigarette Smoke Increases Apoptosis in the Gastric Mucosa: Role of Epidermal Growth Factor

Ma, Li; Wang, Hong Y; Chow, Jennifer; Cho, Chi H.

doi:10.1159/000007692

Cited by 25 publications

(10 citation statements)

References 31 publications

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“…The most plausible explanation for these findings is that smoking causes cellular injury due to oxidative stress. [25][26][27] This is the first report that describes smoke-induced apoptosis in the intestine. It is Smoking alters intestinal apoptosis and GALT S Verschuere et al known that small erosions are found in the FAE of patients with CD.…”

Section: Discussionmentioning

confidence: 92%

Cigarette smoking alters epithelial apoptosis and immune composition in murine GALT

Verschuere

Bracke

Demoor

et al. 2011

Laboratory Investigation

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Smokers have a twofold increased risk to develop Crohn's disease (CD). However, little is known about the mechanisms through which smoking affects CD pathogenesis. Especially Crohn's ileitis is negatively influenced by smoking. Interestingly, the ileum and, more in particular, the Peyer's patches in the terminal ileum are also the sites where the first CD lesions are found. Several chemokines are implicated in the pathogenesis, among which is the CCL20-CCR6 pathway. Here, we studied the gut-associated lymphoid tissue in C57BL/6 wild-type mice and in CCR6-deficient mice after exposure to air or cigarette smoke for 24 weeks. Apoptotic index of the follicle-associated epithelium overlying the Peyer's patches was evaluated. We found that chronic smoke exposure induced apoptosis in the follicle-associated epithelium. Furthermore, immune cell numbers and differentiation along with chemokine expression were determined in Peyer's patches. Important changes in immune cell composition were observed: total dendritic cells, CD4 þ T cells (including regulatory T cells) and CD8 þ T cells increased significantly after smoke exposure. The CD11b þ dendritic cell subset almost doubled. Interestingly, these changes were accompanied by an upregulated mRNA expression of the chemokines CCL9 and CCL20. However, no differences in the increase of dendritic cells were observed between wild-type and CCR6-deficient mice. Our results show that cigarette smoke exposure increases apoptosis in the follicle-associated epithelium and is associated with immune cell accumulation in Peyer's patches.

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Section: Discussionmentioning

confidence: 92%

Cigarette smoking alters epithelial apoptosis and immune composition in murine GALT

Verschuere

Bracke

Demoor

et al. 2011

Laboratory Investigation

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“…These cells were distributed in different regions across the gastric glandular mucosa [14]. The gastritis group had a higher number of apoptotic cells compared to the corresponding control (p < 0.01).…”

Section: Resultsmentioning

confidence: 99%

Relationship between Ethanol-Induced Gastritis and Gastric Ulcer Formation in Rats

Liu

Cho²

2000

Digestion

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Background/Aims: Patients with peptic ulcer diseases have a high prevalence of coexisting chronic gastritis. The mechanism of how gastritis leads to gastric ulcer formation is yet to be determined. The purpose of this study was to clarify the relationship between gastritis and gastric ulcer in rats. Methods: Ethanol (80% v/v, p.o.) was given repeatedly in rats to induce subchronic gastritis. Gastric ulcer was then induced by 60% acetic acid. Results: Findings showed that subchronic gastritis potentiated gastric ulcer formation. It also produced more apoptotic cells, together with an overexpression of tumor necrosis factor-α (TNFα) in the gastric mucosa. Inhibition of the production/release of TNFα by pentoxifylline prevented the increase in apoptosis and the enhancement of susceptibility to ulcerative damage by subchronic gastritis. However, such subchronic gastritis did not further affect the rate of ulcer healing in these animals. Conclusion: The induction of gastritis resulted in an activation of TNFα expression followed by apoptosis in the gastric mucosa. This could lead to an increase in the severity of ulcerative damage in the stomach.

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“…In animal models, cigarette smoke exposure significantly decreased serum epidermal growth factor (EGF) levels (Ma et al, 1999). Although the mechanisms by which cigarette smoke exposure decreases serum EGF are still unknown, depletion of EGF has been associated with reduced gastric blood flow, which in turn, results in the promotion of apoptosis in the gastric mucosa (Ma et al, 1999;Wang et al, 2000). The contents of cigarette smoke may form DNA adducts and induce mutations in tumour suppressor genes (Shin and Cho, 2005).…”

Section: Discussionmentioning

confidence: 99%

Passive smoking and risk of oesophageal and gastric adenocarcinomas

Duan

Sullivan‐Halley

et al. 2009

Br J Cancer

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Few studies have examined the association between passive smoking and the risk of oesophageal and gastric adenocarcinomas. In a population-based case -control study with 2474 participants in Los Angeles County, there was no evidence that passive smoking had any appreciable effect on oesophageal or gastric adenocarcinomas. Tobacco smoking is a well-established cause of oesophageal squamous cell carcinoma (ESCC) and oesophageal adenocarcinoma (EA) (IARC, 2004). Generally, the risk for both types of oesophageal cancer increases with increasing duration of smoking and remains high for a number of years after smoking cessation (IARC, 2004). The literature on smoking and stomach cancer also shows a consistent association with cigarette smoking in both men and women (IARC, 2004;Ladeiras-Lopes et al, 2008). Alcohol drinking is thought to be associated with ESCC (Freedman et al, 2007), but not with EA (Wu et al, 2001), and is not directly related to gastric cancer (Chow, 1999). Although much attention has been focused on the association between active smoking and cancer risk, less has been paid to the association between passive smoking and cancer risk, with the exception of lung cancer (IARC, 2004). A few studies have investigated gastric cancer in relation to passive smoking (Hirayama, 1984;Sandler et al, 1989;Nishino et al, 2001;Mao et al, 2002), but none has reported on EA.We investigated the relationship between passive smoking and the oesophageal and gastric adenocarcinoma (EGA) risks in a population-based case -control study in Los Angeles County. MATERIALS AND METHODSThe details of the study population and design have been described elsewhere (Wu et al, 2001). Briefly, 1716 eligible patients with newly diagnosed first-incident EA, gastric cardia adenocarcinoma (GCA), or distal gastric adenocarcinoma (DGA) between 1992 and 1997 were identified and contacted for participation through the population-based, Los Angeles County Cancer Surveillance Program. Neighbourhood controls were matched individually to each case patient on sex, race, and age ( ± 5 years). To increase statistical power, we sought two controls for each case whenever possible. Inperson interviews were conducted using a structured questionnaire to gather information on demographics, smoking status, smoking history, and household passive smoking exposure during childhood and adulthood. Intensity of passive smoking exposure was measured by the number of smokers who smoked in the participant's presence for at least 1 year and the duration of each exposure. These smokers included the participant's spouse, parents, siblings, or other relatives. Next-of-kin (NOK) were interviewed when case patients were unable to be interviewed due to death or illness. However, we were unable to interview 769 patients who were too ill or died and had no NOK available for interview, whose physicians denied permission to contact, or who refused to participate or could not be located. After excluding participants due to missing information, a total of 938 (220 EA/277 GCA/441 ...

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Cigarette Smoke Increases Apoptosis in the Gastric Mucosa: Role of Epidermal Growth Factor

Cited by 25 publications

References 31 publications

Cigarette smoking alters epithelial apoptosis and immune composition in murine GALT

Cigarette smoking alters epithelial apoptosis and immune composition in murine GALT

Relationship between Ethanol-Induced Gastritis and Gastric Ulcer Formation in Rats

Passive smoking and risk of oesophageal and gastric adenocarcinomas

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