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Induction of TNF, CXCL8 and IL-1 beta in macrophages by Helicobacter pylori secreted protein HP1173 occurs via MAP-kinases, NF-kappa B and AP-1 signaling pathways
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
Stockholm University, Faculty of Science, Department of Molecular Biosciences, The Wenner-Gren Institute.
Number of Authors: 22018 (English)In: Microbial Pathogenesis, ISSN 0882-4010, E-ISSN 1096-1208, Vol. 125, p. 295-305Article in journal (Refereed) Published
Abstract [en]

Macrophages play an important role in the generation of host immune responses against H. pylori. In this study, we investigated the effect of a functionally uncharacterized H. pylori secreted protein HP1173 on macrophage responses. In a screen of eight H. pylori strains, similar expression levels of the HP1173 protein were observed in the whole-cell extracts, however; the amount of protein released into the culture medium varied significantly among strains. Recombinant purified HP1173 (rHP1173) was found to bind to THP-1 cells that were differentiated into macrophages via phorbol-12-myristate-13-acetate (PMA) treatment. The exposure of macrophages to rHP1173 led to the production of the proinflammatory cytokines TNF and IL-1 beta and the chemokine CXCL8 in a dose- and time-dependent manner. Under similar conditions, rHP1173 failed to induce apoptosis in macrophages. Furthermore, rHP1173-induced expression of TNF, IL-1 beta and CXCL8 was observed at the level of gene transcription. Incubation of macrophages in the conditioned medium from a mutant H. pylori strain 26695 lacking HP1173 protein expression resulted in the reduced induction of TNF, CXCL8 and IL-1 beta, confirming the role of the endogenous protein. Intracellular signaling involving MAPKs, NF-kappa B and the AP-1 family of transcription factors was required for rHP1173-induced TNF, CXCL8 and IL-1 beta release from macrophages. The blocking of MyD88, which is an adaptor for multiple toll-like receptors (TLRs), had no effect on rHP1173-induced TNF, CXCL8 and IL-1 beta release from macrophages, suggesting that Myd88-dependent TLR signaling was not involved in the recognition of and responses to rHP1173. These findings provide novel insights into the potential role of HP1173 in H. pylori infection-associated disease development.

Place, publisher, year, edition, pages
2018. Vol. 125, p. 295-305
Keywords [en]
Helicobacter, Secreted proteins, Macrophages, Proinflammatory cytokines, MAPKs
National Category
Biological Sciences Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:su:diva-163597DOI: 10.1016/j.micpath.2018.09.037ISI: 000451792100041PubMedID: 30267894OAI: oai:DiVA.org:su-163597DiVA, id: diva2:1277869
Available from: 2019-01-11 Created: 2019-01-11 Last updated: 2019-01-11Bibliographically approved

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