The Role Of Mannose Receptor In Asthmatic Rats

Part1The expression of mannose receptor in lung of asthmatic model ofratsObjectivesTo observe the expression of mannose receptor in lung tissue of asthmatic rats.Materials and MethodsRats were divided into2groups:1) normal control group;2) asthmatic group.Immunohistochemistry and Western-blot were applied to detect the expression ofMR protein; Real-Time PCR was applied to detect the expression of MR mRNA.ResultsCompared to control group, the expressions of MR mRNA and protein of lung tissuewere significantly increased in asthma group（p＜0.05）.ConclusionsIt is revealed both mRNA and protein expressions of MR are increased in asthmaticrat lung, compared with control. Our results suggested that MR may be related to thepathogenesis of asthma. Part2The mannose receptor expression of alveolar macrophages andairway smooth muscle cells in asthmatic model of rats and the role ofmannose receptor in regulating the endocytosis of alveolarmacrophagesObjectivesTo observe the mannose receptor (MR) expressions on alveolar macrophages (AMs)and airway smooth muscle cells(ASMCs) in asthmatic SD rats, and to investigate therole of MR in regulating the endocytosis of AMs.Materials and MethodsAMs and ASMCs were divided into6groups:1) normal control group(N);2)asthmatic group(A);3) asthmatic+IL-4group(A+I);4) asthmatic+D-(+)-mannosegroup(A+M);5) asthmatic+MR siRNA group(A+R);6) asthmatic+IL-4+D-(+)-mannose group(A+I+M). Immunofluorescence was applied to detect theexpression of MR protein in AMs and ASMCs. The expression of MR mRNA wasdetected by Real-Time PCR. Flow cytometry was used to detect the endocytosisfunction of AMs. The IL-4content of BALF was measured by ELISA.Results1、Compared to control group, the IL-4content of BALF was significantly increasedin asthmatic group, and the difference was statistically significant (p＜0.01).2、Compared to control group, the expressions of AMs MR protein were significantlyincreased in asthmatic and A+M groups, and the difference was statisticallysignificant (p＜0.05). Compared to asthmatic group, with the IL-4interfered, thelevel of AMs MR protein expression was significantly up-regulated(p＜0.01); the expression of AMs MR protein was not significant changed after D-(+)-mannoseintervention; after MR siRNA intervention, the expression of AMs MR proteinwas reduced(p＜0.05); the expression of AMs MR protein was increased withIL-4and D-(+)-mannose, but the difference was not statistically significant(p＞0.05).3、Compared to control group, the endocytosis of AMs was increased in asthmaticrats, and the difference was statistically significant (p＜0.05). Compared toasthmatic group, with the IL-4interfered, the endocytic activity of AMs wasup-regulated(p＜0.05); the endocytosis of AMs was down-regulated afterD-(+)-mannose intervention(p＜0.05); after MR siRNA intervention, theendocytosis of AMs was reduced(p＜0.05); the endocytosis of AMs was reducedwith IL-4and D-(+)-mannose, but the difference was not statistically significant(p＞0.05).4、Compared to control group, the expressions of ASMCs MR protein and mRNAwere significantly increased in asthmatic and A+M groups, and the difference wasstatistically significant (p＜0.05). Compared to asthmatic group, with the IL-4interfered, the level of ASMCs MR protein(p＜0.01) and mRNA(p＜0.05)expressions were up-regulated; the expressions of ASMCs MR protein and mRNAwere not significant changed after D-(+)-mannose intervention; after MR siRNAintervention, the expressions of ASMCs MR protein(p＜0.01) and mRNA(p＜0.05) were reduced; the expression of AMs MR protein and mRNA wereincreased with IL-4and D-(+)-mannose, but the difference was not statisticallysignificant(p＞0.05).ConclusionsIn asthmatic rats, the expressions of AMs and ASMCs MR were increased, and theexpressions were up-regulated by IL-4; the endocytosis of AMs was increasedcompared with control group, and MR is positively related with AMs endocytosis.These results suggest that MR could participate in regulating endocytosis of AMs.