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Associated Gastric Pathology Helicobacter Felis the Development Cellular Immune Responses Are Essential for the Development of Helicobacter felis -Associated Gastric Pathology This information is current as Kevin A. Roth, Sharookh B. Kapadia, Steven M. Martin and of September 26, 2021. Robin G. Lorenz J Immunol 1999; 163:1490-1497; ; http://www.jimmunol.org/content/163/3/1490 Downloaded from References This article cites 47 articles, 14 of which you can access for free at: http://www.jimmunol.org/content/163/3/1490.full#ref-list-1 Why The JI? Submit online. http://www.jimmunol.org/ • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average by guest on September 26, 2021 Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 1999 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. Cellular Immune Responses Are Essential for the Development of Helicobacter felis-Associated Gastric Pathology1 Kevin A. Roth,*† Sharookh B. Kapadia,*‡ Steven M. Martin,*‡ and Robin G. Lorenz2*‡§ The bacteria Helicobacter pylori is a major human pathogen that infects over half of the world’s population. Infection initiates a series of changes in the gastric mucosa, beginning with atrophic gastritis and leading in some patients to peptic ulcer disease, mucosa-associated lymphomas, and gastric adenocarcinoma. Although this cascade of events clearly occurs, little is known about the role of the host immune response in disease progression. We have utilized the C57BL/6 Helicobacter felis mouse model to critically analyze the role of the adaptive immune response in the development of Helicobacter-associated gastric pathology. Infection of B and T cell-deficient RAG-12/2 mice or T cell-deficient TCRbd2/2 mice with H. felis resulted in high levels of colonization, but no detectable gastric pathology. Conversely, infection of B cell-deficient mMT mice resulted in severe gastric alterations identical with those seen in immunocompetent C57BL/6-infected mice, including gastric mucosal hyperplasia and intestinal metaplasia. These results demonstrate that the host T cell response is a critical mediator of Helicobacter-associated Downloaded from gastric pathology, and that B cells and their secreted Abs are not the effectors of the immune-mediated gastric pathology seen after H. felis infection. These results indicate that in addition to specific Helicobacter virulence factors, the host immune response is an important determinant of Helicobacter-associated disease. The Journal of Immunology, 1999, 163: 1490–1497. t has been 14 years since Helicobacter pylori was conclu- One potential host factor is the adaptive immune response, as sively shown to cause acute gastritis (1, 2). Patients infected the gastric inflammatory infiltrate associated with Helicobacter in- http://www.jimmunol.org/ I with H. pylori develop a chronic gastric inflammatory infil- fection is predominantly IgG- and IgA-producing B cells and CD4 trate that primarily affects the antral region. The majority of in- and CD8-positive T cells (9, 10). Initial studies in immunodeficient fections result in no clinical symptoms; however, 10–20% (C.B-17 SCID) mice indicated that the adaptive immune response progress to serious clinical disease. Multiple studies have demon- was not required to maintain chronic gastric inflammation after strated that H. pylori is associated with the development of duo- Helicobacter infection (11). However, recent reports have now denal and gastric ulcer disease, gastric adenocarcinoma, and mu- shown that several mouse strains, including the strain used above, cosa-associated lymphoid tissue (MALT) lymphoma (3–5). The do not develop gastric pathology after Helicobacter infection. Spe- critical factors, either host, bacterial, and/or environmental, that cifically, the inbred mouse strain C57BL/6 develops a severe by guest on September 26, 2021 influence the clinical manifestations of Helicobacter infection are chronic active gastritis and intestinal metaplasia, whereas BALB/c still being elucidated. Some of the observed clinical variation in mouse strains exhibit only mild gastritis after infection with the H. the pathologic response to H. pylori is due to phenotypic and ge- pylori strain SS1 (Cag-A1) and the closely related Helicobacter notypic diversity of the H. pylori bacteria itself, as strains of H. felis (Cag-A2) (12–15). Due to the availability of this new pylori with the cytotoxin-associated gene (cag)3 pathogenicity is- C57BL/6 mouse model of Helicobacter-associated gastric disease, land have been associated with more severe peptic ulcer disease we reevaluated the hypothesis that the host adaptive immune re- (6). However, this correlation does not account for all the mani- sponse initiated by Helicobacter infection is responsible for sub- festations of Helicobacter-induced disease, as MALT lymphomas sequent gastric pathology. are not associated with expression of the cag pathogenicity island, We established gastric infection with H. felis in C57BL/6 wild- and in Far Eastern countries no association between disease out- type and induced mutant mice. H. felis infection in C57BL/6 mice comes and cytotoxin genes has been demonstrated (7, 8). These mimics human disease in many aspects, including a predominant observations suggest that additional factors must interact with H. CD41 T cell response (9, 16) that is associated with an increased pylori to influence the course of gastric disease. epithelial cell proliferative index and hyperplasia (12, 13, 17). However, H. felis does not express the cag pathogenicity island or Departments of *Pathology, †Molecular Biology and Pharmacology, and §Medicine, the vacuolating toxin (vacA), and thus does not itself damage the and ‡Center for Immunology, Washington University School of Medicine, St. Louis, gastric epithelium (18). Induced mutant mouse strains deficient in MO 63110 both B and T cells, or in B cells or T cells alone were infected with Received for publication December 3, 1998. Accepted for publication April 15, 1999. H. felis, and the subsequent gastric pathology was evaluated. In The costs of publication of this article were defrayed in part by the payment of page this report, we demonstrate that the T cell response is crucial for charges. This article must therefore be hereby marked advertisement in accordance Helicobacter-induced gastric pathology, and that post-Helicobac- with 18 U.S.C. Section 1734 solely to indicate this fact. ter infection gastric destruction and hyperproliferation are not me- 1 This study was supported in part by the Charles E. Culpeper Foundation and an Institutional Howard Hughes Medical Institute Pilot Project Award. S.B.K. is sup- diated by B cells or their secreted products. ported by the Division of Biology and Biomedical Sciences, and S.M.M. is supported by a National Institutes of Health Training Grant T32 AI07163. R.G.L. is a Charles E. Culpeper Foundation Scholar. Materials and Methods 2 Address correspondence and reprint requests to: Dr. Robin G. Lorenz, Department Mice of Pathology (Box 8118), Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110. E-mail address: [email protected] C57BL/6J-Rag-1tm1Mom, C57BL/6-Igh-6tm1Cgn, and C57BL/6J-Tcrbtm1Mom tm1Mom 3 Abbreviations used in this paper: cag, cytotoxin associated gene; BrdUrd, 5-bromo- Tcrd breeder pairs were purchased from The Jackson Laboratory 29-deoxyuridine; RAG, recombinase activating gene. (Bar Harbor, ME). The strains were maintained by mating homozygous Copyright © 1999 by The American Association of Immunologists 0022-1767/99/$02.00 The Journal of Immunology 1491 siblings. C57BL/6J control mice were purchased from The Jackson Lab- oratory. Mice were housed in a specific pathogen-free facility in microiso- lator cages under a strictly controlled light cycle and given a standard autoclaved chow diet ad libitum. All mice were maintained in accordance with the guidelines of the Animal Studies Committee of Washington University. Generation of H. felis-induced gastritis H. felis (ATCC 49179; American Type Culture Collection, Manassas, VA) was grown on moist ATCC 260 medium (trypicase soy agar (BBL 11043; Fisher Scientific, Pittsburgh, PA)) supplemented with defibrinated calf blood (5% v/v; Colorado Serum Company, Denver, CO), trimethoprim (5 mg/L; Sigma, St. Louis, MO), vancomycin (6 mg/L; Sigma), and Fun- gizome (1% v/v; Life Technologies, Gaithersburg, MD) under microaero- philic conditions at 37°C for 2 days. Confluent plates of H. felis were harvested, and the number of bacteria were determined by adsorption at 9 OD450, with one OD unit corresponding to 10 bacteria. Bacteria were stored in a mixture of brain heart infusion broth (BHI; Difco 0037; Fisher) and glycerol (31 ml glycerol/100 ml broth) at 270°C. Per os (p.o.) infec- tion of H. felis was accomplished using a 200-ml pipette tip. Mice were inoculated twice over a 3-day period with 0.05 ml of bacterial suspension. Mock infected animals were inoculated with the BHI/glycerol suspension Downloaded from medium. FIGURE 1. Levels of colonization of H. felis in infected C57BL/6, Assessment of H. felis colonization and histopathology 2 2 2 2 mMT, RAG-1 / , and TCRbd / mouse strains. Colonization is repre- Mice were sacrificed and their stomachs rapidly removed. Ninety minutes sented by the H. felis (HF) colonization score, which was based on eval- before sacrifice, animals received an i.p. injection of 5-bromo-29-deoxyuri- uation of immunohistochemical staining of the H. felis organisms as de- dine (BrdUrd; Sigma) (dose, 120 mg/kg) to label cells in S phase (19). scribed in Materials and Methods.
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