Increased Exhaled 8-Isoprostane and Interleukin-6 in Patients with Helicobacter pylori Infection Zeki Yildirim,* Bulent Bozkurt, † Duygu Ozol, † Ferah Armutcu, ‡ Recep Akgedik, § Harun Karamanli, ¶ Deniz Kizilirmak †† and Mustafa _ Ikizek** *Department of Pulmonary Medicine, Gazi University School of Medicine, Ankara, Turkey, † Department of Pulmonary Medicine, Turgut Ozal University, Ankara, Turkey, ‡ Department of Biochemistry, Cerrahpasa School of Medicine, Istanbul University, Istanbul, Turkey, § Department of Pulmonary Medicine, Ordu University School of Medicine, Ordu, Turkey, ¶ Department of Pulmonary Medicine, Ataturk Chest Disease and Chest Surgery Research and Education Hospital, Konya, Turkey, **Department of Internal Medicine, Tatvan State Hospital, Bitlis, Turkey, †† Department of Pulmonary Medicine, Hakkari State Hospital, Hakkari, Turkey Keywords Helicobacter pylori, airway, inflammation, oxidative stress. Reprint request to: Zeki Yildirim, Professor of Pulmonary Medicine, Gazi € University Medical Faculty, Department of Pulmonary Medicine, Ankara, Turkey. E-mail: zekiy@hotmail.com Abstract Background: Helicobacter pylori (H. pylori) infection triggers both local inflammation, usually in gastric mucosa, and chronic systemic inflamma- tion. It is assumed that this local and systemic inflammation is caused by extracellular products excreted by H. pylori. The aim of this study was to investigate the possible association between H. pylori infection and a local inflammatory response in the airway by using exhaled breath condensate technique. Materials and Methods: This study includes 41 H. pylori seropositive patients who have gastric symptoms and 27 healthy control subjects. Pul- monary function tests (PFT), chest X ray, and physical examination were performed in all patients and interleukin-6 (IL-6), 8-isoprostane and nitroty- rosine levels were measured in exhaled breath condensate. Results: Levels of IL-6 and 8-isoprostane in exhaled breath condensate (EBC) were significantly higher in H. pylori positive patients than control subjects (p < 0.05). Nitrotyrosine levels were also higher in H. pylori positive patients but the difference was not statistically significant. Both groups had similar leukocyte counts, C-reactive protein (CRP) levels and PFT parameters. Conclusion: H. pylori infection causes an asymptomatic airway inflammation which can be detected by exhaled breath condensate. The clinical importance of this inflammation remains unclear. Helicobacter pylori (H. pylori) seroprevalence has been widely identified in gastroduodenal diseases [1]. In recent years, its seroprevalence has also been detected in several extragastric disorders such as hematologic dis- eases [2], cardiovascular diseases [3], and chronic otitis [4], and some upper respiratory tract diseases like nasal polyposis [5]. The possible role of the bacterium in the development of extragastric manifestations is unclear [6]. Despite high seroprevalence of H. pylori infection with many inflammatory conditions [7,8], the available data for airway diseases such as COPD [9], chronic bron- chitis [10], and asthma [11] are conflicting. A recent meta-analysis showed weak evidence for an inverse association between asthma and H. pylori infection both in children and in adults [12]. In a study in patients with COPD, the value of forced expiratory volume in 1-sec- ond (FEV 1 ) was found to be lower in patients who were H. pylori-positive than in those who were H. pylori - negative. It was concluded that an association exists between H. pylori and COPD and that H. pylori IgG levels were correlated with the severity of COPD [13]. These findings suggest that H. pylori infection may cause or contribute to airway inflammation. H. pylori infection in the stomach leads to a strong systemic immune response [14]. It is probable that this response has adverse sys- temic effects as well as the gastrointestinal tract. How- ever, it is not known whether H. pylori presence causes asymptomatic inflammation in human airways. © 2016 John Wiley & Sons Ltd, Helicobacter 1 Helicobacter ISSN 1523-5378 doi: 10.1111/hel.12302