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Cis Peptidyl Prolyl Helicobacter Pylori Central TLR4-Dependent NF-κB Activation and Mitogen- and Stress-Activated Protein Kinase 1-Triggered Phosphorylation Events Are Central to Helicobacter pylori Peptidyl Prolyl This information is current as cis-, trans-Isomerase (HP0175)-Mediated of June 26, 2015. Induction of IL-6 Release from Macrophages Sushil Kumar Pathak, Sanchita Basu, Asima Bhattacharyya, Shresh Pathak, Anirban Banerjee, Joyoti Basu and Manikuntala Kundu Downloaded from J Immunol 2006; 177:7950-7958; ; doi: 10.4049/jimmunol.177.11.7950 http://www.jimmunol.org/content/177/11/7950 http://www.jimmunol.org/ References This article cites 46 articles, 24 of which you can access for free at: http://www.jimmunol.org/content/177/11/7950.full#ref-list-1 Subscriptions Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscriptions Permissions Submit copyright permission requests at: http://www.aai.org/ji/copyright.html by guest on June 26, 2015 Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/cgi/alerts/etoc The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 9650 Rockville Pike, Bethesda, MD 20814-3994. Copyright © 2006 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology TLR4-Dependent NF-␬B Activation and Mitogen- and Stress-Activated Protein Kinase 1-Triggered Phosphorylation Events Are Central to Helicobacter pylori Peptidyl Prolyl cis-, trans-Isomerase (HP0175)-Mediated Induction of IL-6 Release from Macrophages1 Sushil Kumar Pathak, Sanchita Basu, Asima Bhattacharyya, Shresh Pathak, Anirban Banerjee, Joyoti Basu, and Manikuntala Kundu2 Helicobacter pylori infection is associated with the local production of chemokines and cytokines, of which IL-6 is overexpressed at the margin of gastric ulcer in H. pylori-positive gastritis. Cells of the monocytic lineage are the major sources of IL-6, and Downloaded from mononuclear cell infiltration in the lamina propria is characteristic of H. pylori-induced chronic infection. Our study shows for the first time that a secreted peptidyl prolyl cis-, trans-isomerase, HP0175 elicits IL-6 gene expression and IL-6 release from macro- phages. An isogenic strain inactivated in the HP0175 gene (knockout) was attenuated in its IL-6-inducing ability, which was restored after complementation with the HP0175 gene. The specificity of the HP0175-induced effect was confirmed by the fact that rHP0175 purified from HEK293 cells could also induce IL-6 release, ruling out the possibility that the observed effect was due to bacterial contaminants. HP0175 was capable of interacting directly with the extracellular domain of TLR4. HP0175-induced IL-6 http://www.jimmunol.org/ gene expression was critically dependent on TLR4-dependent NF-␬B and MAPK activation. TLR4/PI3K-dependent ERK1/2 and p38 MAPK signaling converged upon activation of mitogen- and stress-activated protein kinase 1 (MSK1). The central role of MSK1 was borne out by the fact that silencing of MSK1 expression abrogated HP0175-mediated NF-␬B-dependent IL-6 gene transcription. MSK1 regulated the recruitment of p65 and phopho-Ser10-histone H3 to the IL-6 promoter. HP0175 therefore regulated IL-6 gene transcription through chromatin modification at the IL-6 promoter. The Journal of Immunology, 2006, 177: 7950–7958. elicobacter pylori is a Gram-negative microaerophilic in stimulation of signaling pathways widely involving recruitment bacterium that causes chronic gastritis and also peptic of various adaptor molecules such as MyD88 (11–13), followed by by guest on June 26, 2015 H ulcer, gastric carcinoma, and gastric lymphoma (1). In- the serine/threonine kinase IL-1R-associated kinase 1 (IRAK1)3 fection is associated with the local production of chemokines and (14). IRAK1 becomes phosphorylated, dissociates from the com- cytokines, such as IL-1␤, IL-6, and IL-8 (2, 3). IL-6 is a pleiotropic plex, and associates with TNFR-associated factor 6 (15, 16), fi- cytokine with both pro- and anti-inflammatory properties (4) that is nally leading to the activation of MAPKs, transcription factors overexpressed at the margin of gastric ulcer in H. pylori-positive such as NF-␬B, and concomitant production of cytokines (17, 18). gastritis (5, 6). Its levels are high in H. pylori-infected early gastric The role of TLRs in the response of macrophages during H. pylori cancer and fall significantly after the cure of H. pylori (7). Con- infection has not been studied extensively. TLR4 expression has sidering that activated macrophages are the main sources of IL-6, been reported to be up-regulated in gastric biopsies obtained from it is necessary to understand the effectors of H. pylori driving IL-6 H. pylori-positive patients compared with uninfected controls (19). gene induction in macrophages. Inflammation-associated factors, H. pylori has a large repertoire of secreted proteins, including such as TNF-␣, platelet-derived growth factor, and bacterial en- the best studied virulence factors VacA and CagA. However, the dotoxins, all enhance IL-6 gene expression. clinical outcome of the disease does not necessarily correlate with TLRs play central roles in innate immunity by recognition and the absence or presence of VacA or CagA, making it important to discrimination of specific conserved patterns of molecules derived identify other factors that could modulate the clinical course of the from bacteria, fungi, or viruses (8–10). Activation of TLRs results disease. Till date, urease, and heat shock protein 60 of H. pylori have been reported to induce IL-6 production in macrophages (20, 21). By two-dimensional gel electrophoresis, followed by mass Department of Chemistry, Bose Institute, Kolkata, India spectrometric analysis, Kim et al. (22) have demonstrated the Received for publication January 17, 2006. Accepted for publication September secretion of HP0175, a peptidyl prolyl cis-, trans-isomerase (PPIase), 6, 2006. in the supernatant when H. pylori is grown in vitro. HP0175 is one The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance of the highly and consistently reactive Ags recognized by the sera with 18 U.S.C. Section 1734 solely to indicate this fact. of H. pylori-infected patients (23, 24). It would therefore not be 1 This work was supported in part by grants from the Indian Council of Medical Research and the Department of Atomic Energy (to M.K.). S.K.P. was supported by a fellowship from the Council of Scientific and Industrial Research. 3 Abbreviations used in this paper: IRAK1, IL-1R-associated kinase 1; ChIP, chro- 2 Address correspondence and reprint requests to Dr. Manikuntala Kundu, Depart- matin immunoprecipitation; dn, dominant-negative; ECD, extracellular domain; KO, ment of Chemistry, Bose Institute, 93/1 Acharya Prafulla, Chandra Road, Kolkata knockout; MSK1, mitogen- and stress-activated protein kinase 1; PPIase, peptidyl 700009, India. E-mail address: [email protected] prolyl cis-, trans-isomerase; siRNA, small interfering RNA. Copyright © 2006 by The American Association of Immunologists, Inc. 0022-1767/06/$02.00 The Journal of Immunology 7951 unlikely for this Ag to have a role in the pathogenesis of lease of IL-6 from THP-1 cells. For the expression of His-HP0175 in H. pylori-associated disease. Our previous studies have identified HEK293 cells, the gene encoding HP0175 was cloned between the XbaI HP0175 as a TLR4-interacting protein (25). Because TLR4 is one and EcoRI sites of pcDNA myc-His, followed by transfection in HEK293 cells. HP0175 was purified from the cell lysate by chromatography on of the best studied receptors driving the innate immune response, Ni2ϩ-NTA agarose. we reasoned that it would be worthwhile to explore the effects of HP0175 on macrophage cytokine induction. The study described Complementation of HP0175 in this work provides evidence that H. pylori HP0175 induces the HP0175 was amplified by PCR using the primer pairs 5Ј-GGGGTACCATG release of IL-6 from human macrophages in a TLR4-/MAPK- AAAAAAAATATCTTAAA-3Ј (sense) and 5Ј-GAAGATCTTTACTTGT dependent manner by activating NF-␬B-driven IL-6 gene tran- TGATAACAATT-3Ј (antisense). The resulting PCR product was cloned scription. The contribution of HP0175 in the release of IL-6 was between the KpnI and BglII sites of the shuttle vector pHel2 (a gift from R. Haas, Max von Pettenkofer-Institut fu¨r Hygiene und Medizinische Mikro- confirmed by the observation that an isogenic mutant of H. pylori biologie, Munich, Germany) (28). The shuttle plasmid was introduced into 26695 disrupted in the HP0175 gene was impaired in its ability to the knockout (KO) strain (described in Ref. 25) by natural transformation. release IL-6. Immunodepletion of HP0175 from the aqueous ex- Colonies were selected on plates containing 4 ␮g/ml chloramphenicol ␮ tract of H. pylori also led to the inhibition of IL-6-releasing ability and 10 g/ml kanamycin. and further confirmed the novel role of this protein in the induction Cell culture of cytokine production from macrophages. Chromatin remodeling represents a determining factor control- THP-1 and HEK293 cells were obtained from the National Centre for Cell Science (Pune, India). THP-1 was maintained in RPMI 1640 medium and ling binding of transcription factors and the formation of preini- treated with PMA to induce maturation of the monocytes to a macrophage- tiation complexes. It therefore dictates selective induction of sub- like adherent phenotype, as described (27). Blood was drawn from healthy sets of genes. Our studies present evidence of HP0175 triggering adult volunteers, and PBMC were isolated, as described (27). Downloaded from mitogen- and stress-activated kinase 1 (MSK1)-dependent phos- For treatments with bacteria, H. pylori strains were grown, as described (25), and incubated with PMA-treated THP-1 cells at a multiplicity of phorylation of p65 (RelA) and histone H3.
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