Higher Motility Enhances Bacterial Density and Inflammatory Response in Dyspeptic Patients Infected with Helicobacter pylori Cheng-Yen Kao,* Bor-Shyang Sheu, †,1 Shew-Meei Sheu, † Hsiao-Bai Yang, ‡ Wei-Lun Chang, §,† Hsiu-Chi Cheng † and Jiunn-Jong Wu* ,¶,**,1 *Institute of Basic Medical Sciences, College of Medicine, National Cheng-Kung University, Tainan, Taiwan, † Department of Internal Medicine, College of Medicine, National Cheng-Kung University, Tainan, Taiwan, ‡ Department of Pathology, Ton-Yen General Hospital, Hsinchu, Taiwan, § Department of Clinical Medicine, College of Medicine, National Cheng-Kung University, Tainan, Taiwan, ¶ Department of Medical Laboratory Science and Biotechnology, College of Medicine, National Cheng-Kung University, Tainan, Taiwan, **Center of Infectious Disease and Signaling Research, College of Medicine, National Cheng-Kung University, Tainan, Taiwan Keywords H. pylori, Motility, Pathological outcomes. Reprint requests to: Jiunn-Jong Wu, Department of Medical Laboratory Science and Biotechnology, College of Medicine, National Cheng-Kung University, No. 1, University Rd., Tainan, Taiwan 70101. E-mail: jjwu@mail.ncku. edu.tw 1 These authors contributed equally to this work. Abstract Background: Motility mediated by the flagella of Helicobacter pylori is impor- tant for the cells to move toward the gastric mucus in niches adjacent to the epithelium; then, H. pylori uses the adhesin SabA to interact with sialyl-Le x on inflammatory host cells for persistent infection. Here, we reveal the clinical association of bacterial motility, SabA expression, and pathological outcomes. Methods: Ninety-six clinical isolates were screened for bacterial motility, and the expression of SabA of each isolate was confirmed by Western blot- ting. H. pylori-infected patients were assessed for their bacterial density, sialyl-Le x expression, inflammatory scores, and clinical diseases. Results: The mean diameter in the motility assay was 17 mm, and eight (8.3%) of the strains had impaired motility, with a diameter <5 mm. H. pylori density in cardia, the acute inflammatory score in the body locus, and the prevalence rate of gastric atrophy were increased in patients infected with higher-motility strains (p = .023, <.001, or <.001, respectively). The total inflammatory scores (both acute and chronic) and bacterial density dramati- cally increased in patients expressing the sialyl-Le x antigen and infected with higher-motility, SabA-positive H. pylori (p = .016, .01, or .005, respectively). Conclusion: These results suggest that the higher motility of H. pylori enhances pathological outcomes, and the SabA–sialyl-Le x interaction has a synergistic effect on virulence of the higher-motility strains. Helicobacter pylori is a Gram-negative, spiral-shaped, and microaerophilic bacterium that infects 50% of the pop- ulation worldwide [1]. Persistent infection with H. pylori increases the risk of developing gastroduodenal diseases, including peptic ulcer and gastric adenocarci- noma [2–6]. Successful H. pylori colonization in vivo depends upon bacterial motility to move within the gastric mucus and adhesins to interact with receptors on host cells [7–10]. Several lines of evidence suggest that the motility of H. pylori is an important factor mediating severe infec- tions [11–13]. Lower density of H. pylori and inflamma- tion response has been detected in TK1402 motility mutant-infected gerbils [12]. In addition, Watanabe et al. [13] revealed that higher-motility strains induced more IL-8 secretion of MKN45 cells than lower-motility strains. However, there is limited clinical evidence to support whether motility of H. pylori determines the severity of gastric inflammation in patients. The motility of H. pylori is provided by two to six polar, sheathed flagella that are composed of three main structures: the basal body, the hook and the filament [14]. The H. pylori filament consists of two flagellin pro- teins, the major FlaA and the minor FlaB [15,16]. Such H. pylori flagellin filaments are synthesized, then post- translationally modified intracellularly by glycosylation with a nine carbon pseudaminic acid sugar derivative that resembles sialic acid [17,18]. Deletion of genes responsible for the glycosylation process leads to a loss of late flagellar structures and motility [19]. © 2012 Blackwell Publishing Ltd, Helicobacter 17: 411–416 411 Helicobacter ISSN 1523-5378 doi: 10.1111/j.1523-5378.2012.00974.x