Open AccessIn situ TLR2 and TLR4 expression in a murine model of mycetoma caused by Nocardia brasiliensis
Author(s) -
MillánChiu Blanca Edith,
HernándezHernández Francisca,
PérezTorres Armando,
MéndezTovar Luis Javier,
LópezMartínez Rubén
Publication year - 2011
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1111/j.1574-695x.2010.00775.x
Subject(s) - tlr2 , biology , nocardia brasiliensis , tlr4 , microbiology and biotechnology , proinflammatory cytokine , toll like receptor , immune system , innate immune system , immunology , inflammation , nocardia , nocardiosis , bacteria , genetics
Abstract Actinomycetoma caused by Nocardia brasiliensis is a common disease in tropical regions. This ailment is characterized by a localized chronic inflammation that mainly affects the lower limbs. Toll‐like receptors (TLRs) recognize pathogen‐associated molecular patterns, inducing the production of proinflammatory mediators. The role of TLRs in the immune response against N. brasiliensis is unknown. The aim of this work was to locate and quantify in a murine model the expression of TLR2 and TLR4 in the infection site using reverse transcription‐PCR and immunohistochemistry. The results showed that TLR2 expression increased in the infected tissue, whereas TLR4 expression decreased. The presence of TLR2 and TLR4 was demonstrated in different cell populations throughout the chronic infectious process. In the early stages of this process, TLR2 was expressed in neutrophils and macrophages in direct contact with the inoculum, whereas TLR4 was observed in mast cells. In the advanced stages of the infection, TLR2 was expressed in foam cells and fibroblasts and was likely associated with bacterial containment, while TLR4 was downregulated, probably resulting in an imbalance between the host immune response and the bacterial load that favoured chronic disease.