Human guanylate binding proteins potentiate the anti-chlamydia effects of interferon-gamma.

Chlamydiae are obligate intracellular pathogens that are sensitive to pro-inflammatory cytokine interferon-gamma. IFN-gamma-inducible murine p47 GTPases have been demonstrated to function in resistance to chlamydia infection in vivo and in vitro. Because the human genome does not encode IFN-gamma-in...

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Main Authors: Illya Tietzel, Christelle El-Haibi, Rey A Carabeo
Format: Article
Language:English
Published: Public Library of Science (PLoS) 2009-08-01
Series:PLoS ONE
Online Access:https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0006499&type=printable
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author Illya Tietzel
Christelle El-Haibi
Rey A Carabeo
author_facet Illya Tietzel
Christelle El-Haibi
Rey A Carabeo
author_sort Illya Tietzel
collection DOAJ
description Chlamydiae are obligate intracellular pathogens that are sensitive to pro-inflammatory cytokine interferon-gamma. IFN-gamma-inducible murine p47 GTPases have been demonstrated to function in resistance to chlamydia infection in vivo and in vitro. Because the human genome does not encode IFN-gamma-inducible homologues of these proteins, the significance of the p47 GTPase findings to chlamydia pathogenesis in humans is unclear. Here we report a pair of IFN-gamma-inducible proteins, the human guanylate binding proteins (hGBPs) 1 and 2 that potentiate the anti-chlamydial properties of IFN-gamma. hGBP1 and 2 localize to the inclusion membrane, and their anti-chlamydial functions required the GTPase domain. Alone, hGBP1 or 2 have mild, but statistically significant and reproducible negative effects on the growth of Chlamydia trachomatis, whilst having potent anti-chlamydial activity in conjunction with treatment with a sub-inhibitory concentration of IFN-gamma. Thus, hGBPs appear to potentiate the anti-chlamydial effects of IFN-gamma. Indeed, depletion of hGBP1 and 2 in cells treated with IFN-gamma led to an increase in inclusion size, indicative of better growth. Interestingly, chlamydia species/strains harboring the full-length version of the putative cytotoxin gene, which has been suggested to confer resistance to IFN-gamma was not affected by hGBP overexpression. These findings identify the guanylate binding proteins as potentiators of IFN-gamma inhibition of C. trachomatis growth, and may be the targets of the chlamydial cytotoxin.
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spelling doaj-art-be2785c89c354e768e23eccf8d29254d2025-08-20T02:00:52ZengPublic Library of Science (PLoS)PLoS ONE1932-62032009-08-0148e649910.1371/journal.pone.0006499Human guanylate binding proteins potentiate the anti-chlamydia effects of interferon-gamma.Illya TietzelChristelle El-HaibiRey A CarabeoChlamydiae are obligate intracellular pathogens that are sensitive to pro-inflammatory cytokine interferon-gamma. IFN-gamma-inducible murine p47 GTPases have been demonstrated to function in resistance to chlamydia infection in vivo and in vitro. Because the human genome does not encode IFN-gamma-inducible homologues of these proteins, the significance of the p47 GTPase findings to chlamydia pathogenesis in humans is unclear. Here we report a pair of IFN-gamma-inducible proteins, the human guanylate binding proteins (hGBPs) 1 and 2 that potentiate the anti-chlamydial properties of IFN-gamma. hGBP1 and 2 localize to the inclusion membrane, and their anti-chlamydial functions required the GTPase domain. Alone, hGBP1 or 2 have mild, but statistically significant and reproducible negative effects on the growth of Chlamydia trachomatis, whilst having potent anti-chlamydial activity in conjunction with treatment with a sub-inhibitory concentration of IFN-gamma. Thus, hGBPs appear to potentiate the anti-chlamydial effects of IFN-gamma. Indeed, depletion of hGBP1 and 2 in cells treated with IFN-gamma led to an increase in inclusion size, indicative of better growth. Interestingly, chlamydia species/strains harboring the full-length version of the putative cytotoxin gene, which has been suggested to confer resistance to IFN-gamma was not affected by hGBP overexpression. These findings identify the guanylate binding proteins as potentiators of IFN-gamma inhibition of C. trachomatis growth, and may be the targets of the chlamydial cytotoxin.https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0006499&type=printable
spellingShingle Illya Tietzel
Christelle El-Haibi
Rey A Carabeo
Human guanylate binding proteins potentiate the anti-chlamydia effects of interferon-gamma.
PLoS ONE
title Human guanylate binding proteins potentiate the anti-chlamydia effects of interferon-gamma.
title_full Human guanylate binding proteins potentiate the anti-chlamydia effects of interferon-gamma.
title_fullStr Human guanylate binding proteins potentiate the anti-chlamydia effects of interferon-gamma.
title_full_unstemmed Human guanylate binding proteins potentiate the anti-chlamydia effects of interferon-gamma.
title_short Human guanylate binding proteins potentiate the anti-chlamydia effects of interferon-gamma.
title_sort human guanylate binding proteins potentiate the anti chlamydia effects of interferon gamma
url https://journals.plos.org/plosone/article/file?id=10.1371/journal.pone.0006499&type=printable
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AT reyacarabeo humanguanylatebindingproteinspotentiatetheantichlamydiaeffectsofinterferongamma