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Barley beta‐Glucan and Zymosan induce Dectin‐1 and Toll‐like receptor 2 co‐localization and anti‐leishmanial immune response in Leishmania donovani ‐infected BALB/c mice
Author(s) -
Patidar Ashok,
Mahanty Trishna,
Raybarman Chandan,
Sarode Aditya Y.,
Basak Surajit,
Saha Bhaskar,
Bhattacharjee Surajit
Publication year - 2020
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12952
Subject(s) - zymosan , tlr2 , leishmania donovani , biology , immune system , leishmania , toll like receptor , receptor , effector , glucan , leishmania major , microbiology and biotechnology , immunology , innate immune system , biochemistry , leishmaniasis , visceral leishmaniasis , parasite hosting , world wide web , computer science , in vitro
Toll‐like receptors (TLRs), TLR2 in particular, are shown to recognize various glycans and glycolipid ligands resulting in various immune effector functions. As barley β‐glucan and zymosan are the glycans implicated in immunomodulation, we examined whether these ligands interact with Dectin‐1, a lectin‐type receptor for glycans, and TLR2 and induce immune responses that can be used against Leishmania infection in a susceptible host. The binding affinity of barley β‐glucan and zymosan with Dectin‐1 and TLR2 was studied in silico. Barley β‐glucan‐ and zymosan‐induced dectin‐1 and TLR2 co‐localization was studied by confocal microscopy and co‐immunoprecipitation. These ligands‐induced signalling and effector functions were assessed by Western blot analyses and various immunological assays. Finally, the anti‐leishmanial potential of barley β‐glucan and zymosan was tested in Leishmania donovani ‐infected macrophages and in L. donovani ‐infected BALB/c mice. Both barley β‐glucan and zymosan interacted with TLR2 and dectin‐1, but with a much stronger binding affinity for the latter, and therefore induced co‐localization of these two receptors on BALB/c‐derived macrophages. Both ligandsactivated MyD88‐ and Syk‐mediated downstream pathways for heightened inflammatory responses in L. donovani ‐infected macrophages. These two ligands induced T cell–dependent host protection in L. donovani ‐infected BALB/c mice. These results establish a novel modus operandi of β‐glucans through dectin‐1 and TLR2 and suggest an immuno‐modulatory potential against infectious diseases.