Oral treatment with Hev b 13 prevents experimental arthritis in mice
Author(s) -
Teixeira Larissa De Bortoli,
Epifânio Vera Lúcia Aparecida Aguillar,
Lachat João José,
Foss Norma Tiraboschi,
CoutinhoNetto Joaquim
Publication year - 2012
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.2012.04582.x
Subject(s) - medicine , in vivo , immunology , arthritis , tumor necrosis factor alpha , inflammation , immune system , pharmacology , biology , microbiology and biotechnology
Summary Hev b 13 is an allergenic esterase obtained from the rubber tree Hevea brasiliensis , which has been shown recently to induce human monocytes to release interleukin (IL)‐10 in vitro , and to exert a potent anti‐inflammatory effect in vivo . Moreover, Hev b 13 has been shown to reduce clinical signs of inflammation and also histological damage to the distal colon of mice with 2,4,6‐trinitrobenze sulphonic acid (TNBS)‐induced colitis after its oral administration. The aim of this study was to investigate the effect of Hev b 13 on human mononuclear cells, as well as its therapeutic use in the methylated bovine serum albumin (mBSA) model of antigen‐induced arthritis. Five days before the intra‐articular challenge, and daily thereafter for 8 days, Hev b 13 was administered by oral gavage. In mice treated with a dose of 0·5 mg/kg of Hev b 13, the severity of oedema, leucocyte infiltration, pannus formation and cartilage erosion were reduced significantly. These findings underscore the anti‐inflammatory activity suggested previously for Hev b 13, an activity speculated to be related to its interaction with monocytes/macrophages and the consequent stimulation of IL‐10 release and reduction of tumour necrosis factor (TNF) release. The study also opens a wide range of possible applications in the field of immune‐mediated inflammatory diseases.
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