Ive oxygen metabolites.17 In smokers, the production of oxygen derived free of charge radicals by peripheral PMNs is greater than in non-smokers.18 19 Furthermore, smoking is identified to CD70 Proteins Storage & Stability inhibit the synthesis of gastric mucus and lessen plasma vitamin C concentrations, each of that are eVective scavengers of oxidants developed inside the gastric mucosa.20 These information suggest that oxygen derived free of charge radicals could play a part in each gastric mucosal injury and oxidative DNA damage of gastric epithelial cells in smokers infected with H pylori. Many studies have investigated the eVects of alcohol on H pylori infection. A recent study suggested a protective eVect of alcohol against active H pylori infection.eight This eVect could relate to the antimicrobial eVects of alcohol.21 In our present study, gastric mucosal C-X-C chemokine mRNA expression did not diVer between individuals who did or didn’t consume alcohol, regardless of the truth that ten in the 14 drinkers had been smokers. Despite the fact that these results may CD159a Proteins supplier possibly recommend that alcohol consumption decreases C-X-C chemokine expression, the amount of individuals was insuYcient for additional subgroup evaluation. In conclusion, we have demonstrated an association among smoking and raised gastric C-X-C chemokine expression in H pylori associated gastritis. Increased chemokines could exacerbate the severity of gastritis and aVect the illness outcome in smokers infected with H pylori.Having said that, other prospective confounding variables, which include dietary antioxidant consumption, should be studied to elucidate the eVects of life-style on H pylori connected gastritis.These studies had been undertaken with economic support from Yorkshire Cancer Study plus the European Commission (contract number 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 beneficial 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. five Shimoyama T, Everett SM, Dixon MF, et al. Chemokine mRNA expression in gastric mucosa is linked with Helicobacter pylori cagA positivity and severity of gastritis. J Clin Pathol 1998;51:7650. 6 Endoh K, Leung FW. EVects of smoking and nicotine around the gastric mucosa: a review of clinical and experimental evidence. Gastroenterology 1994:107:8648. 7 Komoto K, Haruma K, Kamada T, et al. Helicobacter pylori infection and gastric neoplasia: correlations with histological gastritis and tumor histology. Am J Gastroenterol 1998;93:1271. 8 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. 10 Dixon MF, Genta RM, Yardley JH, et al. Classification and grading of gastr.
