Mycobacterial infection aggravates Helicobacter pylori-induced gastric preneoplastic pathology by redirection of de novo induced Treg cells.

Autor:	Artola-Borán M; Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland., Fallegger A; Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland., Priola M; Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland., Jeske R; Infection and Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany., Waterboer T; Infection and Cancer Epidemiology, German Cancer Research Center, Heidelberg, Germany., Dohlman AB; Department of Biomedical Engineering, Center for Genomics and Computational Biology, Duke Microbiome Center, Duke University, Durham, NC, USA., Shen X; Department of Biomedical Engineering, Center for Genomics and Computational Biology, Duke Microbiome Center, Duke University, Durham, NC, USA., Wild S; Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland., He J; Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland., Levesque MP; Department of Dermatology, University Hospital Zurich, Zurich, Switzerland., Yousefi S; Institute of Pharmacology, University of Bern, Bern, Switzerland., Simon HU; Institute of Pharmacology, University of Bern, Bern, Switzerland; Department of Clinical Immunology and Allergology, Sechenov University, Moscow, Russia; Laboratory of Molecular Immunology, Institute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russia; Institute of Biochemistry, Medical School Brandenburg, Neuruppin, Germany., Cheng PF; Department of Dermatology, University Hospital Zurich, Zurich, Switzerland., Müller A; Institute of Molecular Cancer Research, University of Zurich, Zurich, Switzerland. Electronic address: mueller@imcr.uzh.ch.
Jazyk:	angličtina
Zdroj:	Cell reports [Cell Rep] 2022 Feb 08; Vol. 38 (6), pp. 110359.
DOI:	10.1016/j.celrep.2022.110359
Abstrakt:	The two human pathogens Helicobacter pylori and Mycobacterium tuberculosis (Mtb) co-exist in many geographical areas of the world. Here, using a co-infection model of H. pylori and the Mtb relative M. bovis bacillus Calmette-Guérin (BCG), we show that both bacteria affect the colonization and immune control of the respective other pathogen. Co-occurring M. bovis boosts gastric Th1 responses and H. pylori control and aggravates gastric immunopathology. H. pylori in the stomach compromises immune control of M. bovis in the liver and spleen. Prior antibiotic H. pylori eradication or M. bovis-specific immunization reverses the effects of H. pylori. Mechanistically, the mutual effects can be attributed to the redirection of regulatory T cells (Treg cells) to sites of M. bovis infection. Reversal of Treg cell redirection by CXCR3 blockade restores M. bovis control. In conclusion, the simultaneous presence of both pathogens exacerbates the problems associated with each individual infection alone and should possibly be factored into treatment decisions. Competing Interests: Declaration of interests The authors declare no competing interests. (Copyright © 2022 The Author(s). Published by Elsevier Inc. All rights reserved.)
Databáze:	MEDLINE
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