Effect of antiallergic herbal agents on chloride channel-3 and immune microenvironment in nasal mucosal epithelia of allergic rhinitis rabbits.
BACKGROUND
Allergic rhinitis (AR) is a Th2 dominant cytokine response. Chloride channel-3 (ClC-3) plays an important role in nasal mucosal edema and inflammatory pathologic changes in AR. Antiallergic herbal agents (AHA) are antiallergic herbal products. In the previous study, we have demonstrated that AHA clearly inhibited allergic medium and relieved allergic reaction of AR. The aim of this study was to evaluate the function of ClC-3 and discuss the possible therapeutic effects of AHA on immune microenvironment in AR.


METHODS
AHA were produced and used to treat AR. An animal model of an AR rabbit was established by ovalbumin (OVA). The rhinitis rabbits were randomly divided into three groups: AHA treated group (AHATG), model group (MG) and healthy control group (HCG). The expressions of ClC-3 protein were examined by immunohistochemical method. The mucosal epithelial cells of all the rabbit groups were primarily cultured with tissue culture method in vitro with or without rhIL-4 or rhIL-2. Furthermore, the expressions of ClC-3 mRNA were detected by real-time PCR. The levels of monocyte chemotactic factor-1 (MCP-1) and vascular cell adhesion molecule-1 (VCAM-1) protein in culture supernatants were measured by ELISA.


RESULTS
The expressions of ClC-3 mRNA increased more in mucosal epithelial cells of MG than those in AHATG and HCG (P < 0.01). The levels of ClC-3 mRNA, MCP-1 and VCAM-1 protein in culture supernatants of MG were significantly higher than those in the other two groups (P < 0.01). Those were significantly increased in MG untreated 12 hours later than those in other two groups (P < 0.01). The expressions of ClC-3 mRNA, MCP-1 and VCAM-1 protein in culture supernatants of MG and HCG treated with rhIL-4 were significantly higher than those in the AHATG treated with rhIL-4 (P < 0.01). The levels of ClC-3 mRNA, MCP-1 and VCAM-1 protein in culture supernatants of all groups treated with rhIL-2 showed no significant changes (P > 0.05).


CONCLUSIONS
AHA can inhibit the secretions of ClC-3, MCP-1 and VCAM-1 in mucosal epithelia and improve inflammatory reaction of AR. ClC-3 plays an important role in the secretion of cytokines and mucosal inflammatory response in AR. RhIL-4 can enhance the secretion of ClC-3, MCP-1 and VCAM-1 in mucosal epithelial cells, especially during the AR process. These enhanced effects of rhIL-4 were significantly suppressed by AHA. The secretions of ClC-3, MCP-1 and VCAM-1 can not be induced obviously by rhIL-2 in mucosal epithelial cells in AR.
Wang
Li-feng
LF
Medical College of Nankai University, Tianjin, China.
Xu
Li-juan
LJ
Guo
Feng-hua
FH
Wang
Li-na
LN
Shen
Xiao-hong
XH
D000818:Animals; D018926:Anti-Allergic Agents / Q000494:pharmacology*; D018932:Chemokine CCL2 / Q000378:metabolism; D018118:Chloride Channels / Q000235:genetics / Q000378:metabolism*; D004797:Enzyme-Linked Immunosorbent Assay; D007150:Immunohistochemistry; D008297:Male; D009092:Mucous Membrane / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D009297:Nasal Mucosa / Q000187:drug effects / Q000276:immunology / Q000378:metabolism*; D016133:Polymerase Chain Reaction; D011817:Rabbits; D011897:Random Allocation; D012220:Rhinitis / Q000139:chemically induced / Q000276:immunology* / Q000378:metabolism*; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism
D018926:Anti-Allergic Agents; D018932:Chemokine CCL2; D018118:Chloride Channels; C115376:ClC-3 channel; D019010:Vascular Cell Adhesion Molecule-1