Ive oxygen metabolites.17 In smokers, the production of oxygen derived no cost radicals by peripheral PMNs is higher than in non-smokers.18 19 Moreover, smoking is identified to inhibit the synthesis of gastric mucus and cut down plasma vitamin C concentrations, each of which are eVective scavengers of oxidants created within the gastric mucosa.20 These data recommend that oxygen derived totally free radicals might play a role in each gastric mucosal injury and oxidative DNA damage of gastric epithelial cells in smokers infected with H pylori. Several studies have investigated the eVects of alcohol on H pylori infection. A recent study recommended a protective eVect of alcohol against active H pylori infection.8 This eVect could relate to the antimicrobial eVects of alcohol.21 In our present study, gastric mucosal C-X-C chemokine mRNA expression didn’t diVer amongst those that did or did not consume alcohol, in spite of the fact that 10 on the 14 drinkers have been smokers. Even though these final results may suggest that alcohol consumption decreases C-X-C chemokine expression, the amount of sufferers was insuYcient for additional subgroup analysis. In conclusion, we have demonstrated an association among smoking and raised gastric C-X-C chemokine expression in H pylori associated gastritis. Elevated chemokines could exacerbate the severity of PI3Kβ Synonyms gastritis and aVect the disease outcome in smokers infected with H pylori.Nonetheless, other possible confounding components, for instance dietary antioxidant consumption, should be studied to elucidate the eVects of life-style on H pylori linked gastritis.These research have been undertaken with economic support from Yorkshire Cancer Analysis and the European Commission (contract quantity ICA4-CT-19990010). We thank Dr I Lindley of Novartis for giving GRO primers and Dr S Farmery for useful discussion. The authors thank Professor A Munakata and Dr S Nakaji for their helpful discussion.1 Luster AD. Mechanisms of illness: chemokines– chemotactic cytokines that mediate inflammation. N Engl J Med 1998:338:4365. two Crabtree JE, Peichl P, Wyatt JI, et al. Gastric IL-8 and IL-8 IgA autoantibodies in Helicobacter pylori infection. Scand J Immunol 1993:37:650. three Peek RM, Miller GG, Tham KT, et al. Heightened inflammatory response and cytokine expression in vivo to CagA+ Helicobacter pylori strains. Lab Invest 1995:73: 7600. four Ando T, Kusugami K, Ohsuga M, et al. Interleukin-8 activity correlates with histological severity in Helicobacter pylori-associated antral gastritis. Am J Gastroenterol 1996: 91:1150. 5 Shimoyama T, Everett SM, Dixon MF, et al. Chemokine mRNA expression in gastric mucosa is associated with Helicobacter pylori cagA positivity and severity of gastritis. J Clin Pathol 1998;51:7650. six Endoh K, Leung FW. EVects of smoking and nicotine around the gastric mucosa: a overview of clinical and experimental proof. Gastroenterology 1994:107:8648. 7 Komoto K, Haruma K, Kamada T, et al. Helicobacter pylori β-lactam supplier infection and gastric neoplasia: correlations with histological gastritis and tumor histology. Am J Gastroenterol 1998;93:1271. eight Brenner H, Rothenbacher D, Bode G, et al. Relation of smoking and alcohol and coVee consumption to active Helicobacter pylori infection. BMJ 1997:315:14892. 9 Morrison D, Strieter RM, Donnelly SC, et al. Neutrophil chemokines in bronchoalveolar lavage fluid and leukocyteconditioned medium from nonsmokers and smokers. Eur Respir J 1998;12:10672. ten Dixon MF, Genta RM, Yardley JH, et al. Classification and grading of gastr.
