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Interaction of Fasciola hepatica Fatty Acid Binding Protein with TLR‐2: A preliminary study to understand the immunomodulation mechanisms that exert F. hepatica on the immune system (LB287)
Author(s) -
RuizJiménez Caleb,
Espino Ana
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.lb287
Subject(s) - cd14 , immune system , tlr2 , fasciola hepatica , biology , innate immune system , toll like receptor , immunology , receptor , inflammation , secretion , microbiology and biotechnology , biochemistry , helminths
In the last decade scientists have shown interest to the strong anti‐inflammatory role that exhibit some helminthes parasites. Fasciola hepatica , is able to induce long‐lasting chronic disease in the mammalian host associated to predominant Th2 responses, which is linked to an anti‐inflammatory phenotype. For this purpose, parasite secrete and express on its surface a large number of proteins that are necessary for their metabolism, and, in addition, it has the ability to modulate the host’s immune response. One of these proteins is fatty acid binding protein (FABP), a protein family of 12kDa that play an essential role in the lipid metabolisms. Recently, our group demonstrated that FABP is able to block the inflammatory cytokine storm typically induced by LPS from Gram‐negative bacteria through the Toll‐like receptor 4 (TLR‐4) and thereby is able to prevent the septic shock in mice. In this work, using HEK‐TLR2 and THP1‐Blue CD14 cells we demonstrated that FABP is also able to block the activation of TLR2 typically produced by specific TLR2‐ligand in a manner that is dose dependent. In addition, in all cases where cells were exposed to FABP prior stimulation with specific TLR2‐ligand the production of inflammatory and pro‐inflammatory cytokines resulted in significant suppression. These results demonstrate that FABP may have a suppressive effect on cells of immune system targeting multiple TLR pathways.