HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Akhiani, A. A. Articles by Lycke, N. Y. Search for Related Content PubMed PubMed Citation Articles by Akhiani, A. A. Articles by Lycke, N. Y.

IgA Antibodies Impair Resistance against Helicobacter pylori Infection: Studies on Immune Evasion in IL-10-Deficient Mice¹

Department of Clinical Immunology, Göteborg University, Göteborg, Sweden

We recently reported that Helicobacter pylori-specific Abs impair the development of gastritis and down-regulate resistance against H. pylori infection. In this study, we asked whether IgA Abs specifically can have an impact on H. pylori colonization and gastric inflammation. To obtain a sensitive model for the study of inflammation we crossed IgA- and IL-10-deficient mice. We found that IL-10^–/–/IgA^–/– mice were significantly less colonized than IL-10^–/–/IgA^+/+ mice, which in turn were less colonized than wild-type (WT) mice. The IL-10^–/–/IgA^–/– mice exhibited a 1.2-log reduction in bacterial counts compared with that in IL-10^–/–/IgA^+/+ mice, suggesting that IgA Abs rather promoted than prevented infection. The reduced colonization in IL-10^–/–/IgA^–/– mice was associated with the most severe gastritis observed, albeit all IL-10^–/– mice demonstrated more severe gastric inflammation than wild-type mice. The gastritis score and the infiltration of CD4⁺ T cells into the gastric mucosa were significantly higher in IL-10^–/–/IgA^–/– mice than in IL-10^–/–/IgA^+/+ mice, arguing that IgA Abs counteracted inflammation. Moreover, following oral immunization, IL-10^–/–/IgA^–/– mice were significantly better protected against colonization than IL-10^–/–/IgA^+/+ mice. However, the stronger protection was associated with more severe postimmunization gastritis and gastric infiltration of CD4⁺ T cells. There was also a clear increase in complement receptor-expressing cells in IL-10^–/–/IgA^–/– mice, though C3b-fragment deposition in the gastric mucosa was comparable between the two. Finally, specific T cell responses to recall Ag demonstrated higher levels of IFN- production in IL-10^–/–/IgA^–/– as compared with IL-10^–/–/IgA^+/+ mice. Thus, it appears that IgA and IL-10 help H. pylori bacteria evade host resistance against infection.

This article has been cited by other articles:

				D. N. Wolfe, G. S. Kirimanjeswara, E. M. Goebel, and E. T. Harvill Comparative Role of Immunoglobulin A in Protective Immunity against the Bordetellae Infect. Immun., September 1, 2007; 75(9): 4416 - 4422. [Abstract] [Full Text] [PDF]

				J. M. Taylor, M. E. Ziman, J. Fong, J. V. Solnick, and M. Vajdy Possible Correlates of Long-Term Protection against Helicobacter pylori following Systemic or Combinations of Mucosal and Systemic Immunizations Infect. Immun., July 1, 2007; 75(7): 3462 - 3469. [Abstract] [Full Text] [PDF]

				K. Kiriya, N. Watanabe, A. Nishio, K. Okazaki, M. Kido, K. Saga, J. Tanaka, T. Akamatsu, S. Ohashi, M. Asada, et al. Essential role of Peyer's patches in the development of Helicobacter-induced gastritis Int. Immunol., April 1, 2007; 19(4): 435 - 446. [Abstract] [Full Text] [PDF]