Ive oxygen metabolites.17 In smokers, the production of oxygen derived no cost radicals by peripheral PMNs is greater than in non-smokers.18 19 Moreover, smoking is known to inhibit the synthesis of gastric mucus and lower plasma vitamin C concentrations, each of that are eVective scavengers of oxidants produced inside the gastric mucosa.20 These data suggest that oxygen derived totally free radicals may well play a role in both gastric mucosal injury and oxidative DNA harm of gastric epithelial cells in smokers infected with H pylori. Several studies have investigated the P2X3 Receptor site 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 towards the antimicrobial eVects of alcohol.21 In our present study, gastric mucosal C-X-C chemokine mRNA expression did not diVer between those who did or didn’t consume alcohol, in spite of the fact that 10 of your 14 drinkers were smokers. While these results could recommend that alcohol consumption decreases C-X-C chemokine expression, the number of individuals was insuYcient for additional subgroup evaluation. In conclusion, we have demonstrated an association involving smoking and raised gastric C-X-C chemokine expression in H pylori associated gastritis. Enhanced chemokines may well exacerbate the severity of gastritis and aVect the illness outcome in smokers infected with H pylori.Even so, other possible confounding factors, which include dietary antioxidant consumption, ought to be studied to elucidate the eVects of lifestyle on H pylori linked gastritis.These studies had been undertaken with financial support from Yorkshire Cancer Investigation plus the European Commission (contract number ICA4-CT-19990010). We thank Dr I Lindley of Novartis for offering GRO primers and Dr S Farmery for beneficial discussion. The authors thank Professor A Munakata and Dr S Nakaji for their helpful discussion.1 Luster AD. Mechanisms of illness: chemokines– chemotactic TLR2 Formulation cytokines that mediate inflammation. N Engl J Med 1998:338:4365. 2 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. 4 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. 6 Endoh K, Leung FW. EVects of smoking and nicotine around the gastric mucosa: a evaluation 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. 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. 10 Dixon MF, Genta RM, Yardley JH, et al. Classification and grading of gastr.
