| Bronchial asthma is chronic airway inflammation in which many kinds of cells (mast cells, T lymphocytes, the neutral type of cells, airway epithelial cells) and cytokines are involved. The incidence of asthma has increased in westernized societies [1], young adults at a rate of 5-6%, especially there has an increase in children asthma, but also an increase in fatal asthma [2]. Researches show that different chemokines play their specific roles at different stages of asthma.Intelectin is composed of calcium-dependent galactose binding lectins, it is divided into intelectin-1 and intelectin-2, it was first found in small intestinal paneth cells. It suggested that it played a role resistance against bacterial infection. Human intelectin-1 was subsequently found in the human body, intelectin protein is a secreted glycoprotein that contains 295 amino acids and N-connection oligosaccharides, its basic structure is 120KD trimer [3]. In our previous research, by Real time-PCR detection the level of intelectin mRNA was increased in mouse lung tissue that sensitized by eggs in mouse asthma model, it also contains over secretion airway mucus protein. Other papers reported in patients with mucinous adenocarcinoma in the colon, IL-4 and IL-13 can cause human intelectin-1 over expression [4]. Human intelectin-1 expresses in heart, small intestine, colon and other organs, compared with mouse intelectin they have a high degree of homology. Omentin is a recently identified secreted protein which highly expresses in visceral fat and subcutaneous adipose [5]. Omentin divides into omentin-1 and omentin-2; both of them have 83% identical acids [6]. It can express in other tissues at low level, it is also known as intelectin. Being allergic is a common health problem, CD4+Tcells involve in chronic allergic diseases, Th1 cell mainly secretes LFN-r, and Th2 cell regulates reaction by secreting IL-4, IL-5 and IL-13[7]. The differentiation of T h cells is determined by innate immune system and its cytokines [8]. CC chemokines and Th2 cytokines play a key role in asthma and other immune diseases, especially IL-4 and IL-13[9]. Because IL-13 can regulate eosinophils inflammation and mucus generation, so it is considered as one of the key factors in asthma [10].CD4+T cells differentiate into Th1 and Th2 finally, the levels of these cytokines (IL-2, IL-4, IL-5, IL-13, GM-CSF and IFN-γ) decide the way of CD4+T cells differentiation into [11]. Cytokines control T cells differentiation strictly through mitosis. We can understand the relation between proliferation and differentiation by exploring these genes. There is no correlation between IL-2 initial expression and cell cycle, the expression of IFN-γneeds constantly split. IL-4 expression requires three cell division [12]. Exposed to antigen airway epithelial cells can not give priority to start the Th2 cells, it has been reported that Th1 cells can promote Th2 cells response by mediated antigen [13]. Pathogenesis of asthma suggests part of T cell factors involved in, including IL-4 and its receptors, blocking the way of IL-13 can reduce the asthma inflammation [14]. At parasite infection in the mutant IL-4(IL-4/-) mouse model, we found that Th2 cells could not be activated, it decreases the expression of IL-5 andIL-9[15].In our previous research about mouse asthma model: we found that the levels of intelectin-1 and intelectin-2 mRNA were increased, we could see the secretion of mucus protein was increased by immunohistochemistry, the number of eosinophils was increased in lavage fluid. In order to explore the expression of intelectin in asthmatic patients, we collected the serum of asthma group and normal group. We observed the level of intelectin-1 in both groups to explore the correlation between IL-13 and intelectin-1, whether both of them were at high level, so we will explore if iltelectin-1 promotes CD4+T cell differentiation. The aim is that well understanding the role of intelectin-1 plays part in. This research is divided into two parts: PartⅠIntelcetin-1 level in plasma of patients with acute asthma exacerbationPurpose: To explore the level of intelectin-1 and IL-13 in patients'plasma with asthma.Method: (1) To collect peripheral blood serum as samples, the samples were divided into asthma group (n=16) and normal group (n=19). (2) To detect the pulmonary function of each sample. (3) Intelectin-1 was detected by ELISA. (4) IL-13 was detected by ELISA.Results: (1) Compared with normal group lung function of asthma group was decreased (p<0.05). (2) Compared with normal group intelectin-1 level was elevated in the plasma of asthma group (p<0.05). (3) Compared normal group IL-13 level was elevated in the plasma of asthma group (p<0.05).Conclusion: The intelectin-1 levels were elevated in plasma of asthma group, there was no significant correlation between intelectin-1 and lung function in asthma group. PartⅡThe role of intelectin-1 in CD4+ T lymphocytes differentiationPurpose: To explore the mechanism of intelectin-1 takes part in mouse CD4+T cells differentiation.Method: (1) Make conditioned medium (2) CD4+Tcells were sterile isolated from mouse spleen and divided into control group and condition media group.Results: (1) Compared with the control group IL-5 mRNA of the group incubated with intelectin-1 was high expressed (p<0.05). (2) Compared with the control group the levels of IFN–r and TNF-αshowed no significant decrease.Conclusion: CD4+Tcells differentiation was consequence to intelectin-1, intelectin-1 promotes Th2 cells differentiation, but there was no evidence could prove intelectin-1 promotes Th1 cells differentiation. |
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