Analysis of the expression of toll-like receptors 2 and 4 and cytokine production during experimental Leishmania chagasi infection
Toll-like receptors (TLRs) recognise pathogen-derived molecules and influence immunity to control parasite infections. This study aimed to evaluate the mRNA expression of TLRs 2 and 4, the expression and production of the cytokines interleukin (IL)-12, interferon (IFN)-γ, tumor necrosis factor (TNF)...
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Veröffentlicht in: | Memórias do Instituto Oswaldo Cruz 2011-08, Vol.106 (5), p.573-583 |
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Zusammenfassung: | Toll-like receptors (TLRs) recognise pathogen-derived molecules and
influence immunity to control parasite infections. This study aimed to
evaluate the mRNA expression of TLRs 2 and 4, the expression and
production of the cytokines interleukin (IL)-12, interferon
(IFN)-γ, tumor necrosis factor (TNF)-α, IL-17, IL-10 and
transforming growth factor (TGF)-β and the production of nitric
oxide (NO) in the spleen of mice infected with Leishmania chagasi. It
also aimed to evaluate any correlations between mRNA expression TLR2
and 4 and cytokines and NO production. Infection resulted in increased
TLR2-4, IL-17, TNF-α and TGF-β mRNA expression during early
infection, with decreased expression during late infection correlating
with parasite load. IFN-γ and IL-12 mRNA expression decreased at
the peak of parasitism. IL-10 mRNA expression increased throughout the
entire time period analysed. Although TGF-β, TNF-α and IL-17
were highly produced during the initial phase of infection, IFN-γ
and IL-12 exhibited high production during the final phase of
infection. IL-10 and NO showed increased production throughout the
evaluated time period. In the acute phase of infection, there was a
positive correlation between TLR2-4, TNF-α, IL-17, NO, IL-10 and
TGF-β expression and parasite load. During the chronic phase of
infection, there was a positive correlation between TLR2-4, TNF-α,
IL-17 and TGF-β expression and parasite load. Our data suggest
that infection by L. chagasi resulted in modulation of TLRs 2 and 4 and
cytokines. |
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ISSN: | 1678-8060 0074-0276 1678-8060 0074-0276 |
DOI: | 10.1590/S0074-02762011000500010 |