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A recombinant cystatin from Ascaris lumbricoides attenuates inflammation of DSS‐induced colitis
Author(s) -
Coronado S.,
Barrios L.,
Zakzuk J.,
Regino R.,
Ahumada V.,
Franco L.,
Ocampo Y.,
Caraballo L.
Publication year - 2017
Publication title -
parasite immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 75
eISSN - 1365-3024
pISSN - 0141-9838
DOI - 10.1111/pim.12425
Subject(s) - ascaris lumbricoides , inflammation , cystatin , colitis , myeloperoxidase , inflammatory bowel disease , immunology , medicine , biology , cystatin c , helminths , disease , creatinine
Summary Helminthiasis may ameliorate inflammatory diseases, such as inflammatory bowel disease and asthma. Information about immunomodulators from Ascaris lumbricoides is scarce, but could be important considering the co‐evolutionary relationships between helminths and humans. We evaluated the immunomodulatory effects of a recombinant cystatin from A. lumbricoides on an acute model of dextran sodium sulphate ( DSS )‐induced colitis in mice. From an A. lumbricoides cDNA library, we obtained a recombinant cystatin ( rA l‐ CPI ). Protease activity inhibition was demonstrated on cathepsin B and papain. Immunomodulatory effects were evaluated at two intraperitoneal doses (0.5 and 0.25 μg/G) on mice with DSS ‐induced colitis. Body weight, colon length, Disease Activity Index ( DAI ), histological inflammation score, myeloperoxidase ( MPO ) activity, gene expression of cytokines and cytokines levels in colon tissue were analysed. Treatment with rA l‐ CPI significantly reduced DAI , MPO activity and inflammation score without toxic effects. Also, IL ‐10 and TGF ‐B gene overexpression was observed in rA l‐ CPI ‐treated group compared to DSS ‐exposed control and healthy mice. Furthermore, a reduction in IL ‐6 and TNF ‐A expression was found, and this was confirmed by the levels of these cytokines in colonic tissue. In conclusion, rA l‐ CPI reduces inflammation in a mouse model of DSS ‐induced colitis, probably by increasing the expression of anti‐inflammatory cytokines and reducing pro‐inflammatory ones.