Characterization of the In Vitro Chlamydia pecorum Response to Gamma Interferon
is an important intracellular bacterium that causes a range of diseases in animals, including a native Australian marsupial, the koala. In humans and animals, a gamma interferon (IFN-γ)-mediated immune response is important for the control of intracellular bacteria. The present study tested the hypo...
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Veröffentlicht in: | Infection and immunity 2018-04, Vol.86 (4) |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | is an important intracellular bacterium that causes a range of diseases in animals, including a native Australian marsupial, the koala. In humans and animals, a gamma interferon (IFN-γ)-mediated immune response is important for the control of intracellular bacteria. The present study tested the hypotheses that
can escape IFN-γ-mediated depletion of host cell tryptophan pools. In doing so, we demonstrated that, unlike
,
is completely resistant to IFN-γ in human epithelial cells. While the growth of
was inhibited in tryptophan-deficient medium, it could be restored by the addition of kynurenine, anthranilic acid, and indole, metabolites that could be exploited by the gene products of the
tryptophan biosynthesis operon. We also found that expression of
genes was detectable only when
was grown in tryptophan-free medium, with gene repression occurring in response to the addition of kynurenine, anthranilic acid, and indole. When grown in bovine kidney epithelial cells, bovine IFN-γ also failed to restrict the growth of
, while
was inhibited, suggesting that
could use the same mechanisms to evade the immune response
in its natural host. Highlighting the different mechanisms triggered by IFN-γ, however, both species failed to grow in murine McCoy cells treated with murine IFN-γ. This work confirms previous hypotheses about the potential survival of
after IFN-γ-mediated host cell tryptophan depletion and raises questions about the immune pathways used by the natural hosts of
to control the widespread pathogen. |
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ISSN: | 0019-9567 1098-5522 |
DOI: | 10.1128/IAI.00714-17 |