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Gu N.,Huazhong University of Science and Technology | Gu N.,Key Laboratory of Respiratory Diseases | Kang G.,Huazhong University of Science and Technology | Kang G.,Key Laboratory of Respiratory Diseases | And 9 more authors.
American Journal of Physiology - Lung Cellular and Molecular Physiology | Year: 2010

Asthma is characterized by airway inflammation, mucus overproduction, airway hyperreactivity, and peribronchial fibrosis. Intelectin has been shown to be increased in airway epithelium of asthmatics. However, the role of intelectin in the pathogenesis of asthma is unknown. Airway epithelial cells can secrete chemokines such as monocyte chemotactic protein (MCP)-1 and -3 that play crucial roles in asthmatic airway inflammation. We hypothesized that intelectin plays a role in allergic airway inflammation by regulating chemokine expression. In a mouse allergic asthma model, we found that mRNA expression of intelectin-2 as well as MCP-1 and -3 in mouse lung was increased very early (within 2 h) after allergen challenge. Expression of intelectin protein was localized to mucous cells in airway epithelium. Treatment of MLE12 mouse lung epithelial cells with interleukin IL-13, a critical mediator of allergic airway disease, induced expression of intelectin-1 and -2 as well as MCP-1 and -3. When IL-13-induced intelectin-1 and -2 expression was inhibited by RNA interference, IL-13-induced extracellular signal-regulated kinase 1/2 phosphorylation and MCP-1 and -3 production by MLE12 cells was inhibited. Furthermore, inhibition of intelectin expression by airway transfection with shRNA targeting intelectin-1 and -2 attenuated allergeninduced airway inflammation. We conclude that intelectin, a molecule expressed by airway epithelial cells and upregulated in asthma, is required for IL-13-induced MCP-1 and -3 production in mouse lung epithelial cells and contributes to allergic airway inflammation. Copyright © 2010 the American Physiological Society.


Cheng D.,Huazhong University of Science and Technology | Cheng D.,Key Laboratory of Respiratory Diseases | Zhang K.,Huazhong University of Science and Technology | Zhang K.,Key Laboratory of Respiratory Diseases | And 3 more authors.
American Journal of Medical Genetics, Part B: Neuropsychiatric Genetics | Year: 2014

X-box binding protein 1 (XBP1) is a pivotal transcription factor and plays an important role in the pathogenesis of psychiatric illness. The association between XBP1 -116C/G polymorphism and risk of psychiatric illness has been investigated in different populations. However, the results of these studies remain conflicting. Therefore, we performed a systematic meta-analysis to evaluate the association between XBP1 -116C/G polymorphism and the overall psychiatric illness risk. Pubmed, Embase, and Chinese Biomedical Literature Database (CBM) were searched for case-control studies on the association between XBP1 -116C/G polymorphism and psychiatric illness risk published up to July 31, 2014. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to access the strength of this association. Fourteen case-control studies including 3,512 cases and 4,889 controls were included. Overall, no significant association was found between XBP1 -116C/G polymorphism and the risk of psychiatric illness (C/G vs. C/C: OR=1.04, 95%CI=0.92-1.17, P=0.54). However, there was a significant association between this polymorphism and the psychiatric illness in Asian population (C/G vs. C/C: OR=1.27, 95%CI=1.00-1.61, P=0.05; G/G+C/G vs. C/C: OR=1.32, 95%CI=1.05-1.65, P=0.02). Furthermore, we found a significant association between XBP1 -116C/G polymorphism and the risk of bipolar disorder in Asian population (C/G vs. C/C: OR=1.81, 95%CI=1.15-2.86, P=0.01). The XBP1 -116C/G polymorphism is associated with an increased risk of bipolar disorder in Asian population. © 2014 Wiley Periodicals, Inc.


Cheng D.,Huazhong University of Science and Technology | Cheng D.,Key Laboratory of Respiratory Diseases | Di H.,Huazhong University of Science and Technology | Di H.,Key Laboratory of Respiratory Diseases | And 3 more authors.
Internal Medicine | Year: 2015

Objective: To comprehensively evaluate the association between the CC16 gene A38G polymorphism and the risk of asthma.Methods: Studies were retrieved from databases including PubMed, EMBASE, Web of Science and the Chinese Biomedical Literature Database according to the inclusive and exclusive criteria. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of the associations.Materials: Fifteen case-control studies with 1,623 cases and 3,294 controls were recruited for the analysis of the association between the CC16 gene A38G polymorphism and the risk of asthma.Results: The overall ORs showed no significant associations between the CC16 gene A38G polymorphism and the risk of asthma (AA vs. GG: OR=1.04, 95%CI=0.86-1.25; AG vs. GG: OR=1.08, 95%CI=0.94-1.24; AA + AG vs. GG: OR=1.07, 95%CI=0.94-1.22; AA vs. AG + GG: OR=1.01, 95%CI=0.85-1.19; A vs. G: OR=1.04, 95%CI=0.95-1.14). Moreover, similar results were obtained in the subgroup analysis stratified by ethnicity (Asian: AG vs. GG: OR=1.02, 95%CI=0.87-1.21; Caucasian: AG vs. GG: OR=1.22, 95%CI=0.94- 1.57) and age (Child: AG vs. GG: OR=1.21, 95%CI=0.84-1.74; Adult: AG vs. GG: OR=1.06, 95%CI=0.91- 1.23).Conclusion: CC16 gene A38G polymorphism is not associated with the risk of asthma. © 2015 The Japanese Society of Internal Medicine. All rights reserved.


Zhang K.,Huazhong University of Science and Technology | Zhang K.,Key Laboratory of Respiratory Diseases | Yi L.,Huazhong University of Science and Technology | Yi L.,Key Laboratory of Respiratory Diseases | And 6 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2016

Background: Toll-like receptor 2 (TLR2) gene plays an important role in the pathogenesis of pulmonary tuberculosis and tuberculous meningitis. The association between TLR2 T597C polymorphism and the susceptibility to pulmonary tuberculosis has been extensively studied. However, the results of these studies remain inconsistent. Therefore, we performed a meta-analysis to evaluate the association between TLR2 T597C polymorphism and the susceptibility to pulmonary tuberculosis and tuberculous meningitis. Methods: PubMed, Embase, CNKI, Wanfang, Weipu databases were searched for case-control studies on TLR2 polymorphisms and the risks of tuberculosis, published up to Nov 31, 2014. To assess the strength of the association between TLR2 polymorphism and pulmonary tuberculosis and tuberculous meningitis, the odds ratios (ORs) with 95% confidence intervals (CIs) were used. The meta-analysis of the associations between the TLR2 T597C polymorphism and pulmonary tuberculosis and tuberculous meningitis were carried out under different genetic models. Results: Fourteen published studies with 4381 cases and 5082 controls were included. Overall, there are significant association between TLR2 T597C polymorphism and the risk of tuberculosis (CC vs. TC OR = 1.26, 95% CI = 1.10-1.43; CC vs. TT OR = 1.20, 95% CI = 1.04-1.38; CC vs. TC+TT OR = 1.23, 95% CI = 1.08-1.39). When stratified by ethnicity, we found a significant association between this polymorphism and tuberculosis risks in Asian (CC vs. TC OR=1.23, 95% CI = 1.02-1.48; CC vs. TT OR = 1.22, 95% CI = 1.12-1.47; CC vs. TC+TT OR = 1.22, 95% CI = 1.02-1.46) and Caucasians (CC vs. TC OR = 1.31, 95% CI = 1.01-1.62; CC vs. TC+TT OR = 1.24, 95% CI = 1.01-1.52). We also found significant the association between this polymorphism and pulmonary tuberculosis (CC vs. TC OR = 1.16, 95% CI = 1.01-1.34) and the tuberculous meningitis (CC vs. TC OR = 3.16, 95% CI = 2.00-5.00; CC vs. TT OR = 3.56, 95% CI = 2.27-5.58; CC vs. TC+TT OR = 3.37, 95% CI = 2.19-5.19; CC+TC vs. TT OR = 1.36, 95% CI = 1.05-1.77; C vs. T OR = 1.52, 95% CI = 1.25-1.85), respectively. Conclusions: TLR2 T597C polymorphism associated with the susceptibility to pulmonary tuberculosis and tuberculous meningitis. © 2016, E-Century Publishing Corporation. All rights reserved.


Zhang K.,Huazhong University of Science and Technology | Zhang K.,Key Laboratory of Respiratory Diseases | Cheng D.,Huazhong University of Science and Technology | Cheng D.,Key Laboratory of Respiratory Diseases | And 6 more authors.
International Journal of Clinical and Experimental Pathology | Year: 2014

Background: Angiotensin I-converting enzyme (ACE) gene plays an important role in the pathogenesis of cancers. The association between ACE insertion/deletion (I/D) polymorphism and the risk of various cancers has been studied. However, the results of these studies remain conflicting. Therefore, we performed a meta-analysis to evaluate the association between ACE I/D polymorphism and the risk of cancers. Methods: PubMed, Embase, ScienceDirect, Springer, CNKI, Wanfang, Weipu, CBM databases and Google Scholar were searched for case-control studies on ACE I/D polymorphism and the risk of cancers, published up to Dec 31, 2013. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of the association between ACE I/D polymorphism and cancer risk. Results: Thirty-five published studies with 5007 cases and 8173 controls were included. Overall, there were no significant association between ACE I/D polymorphism and the risk of cancers (II vs. ID+DD OR = 1.05, 95% CI = 0.89-1.23, I vs. D OR = 1.00, 95% CI = 0.89-1.13). However, when stratified by ethnicity, we found a significant association between this polymorphism and cancer risk in Caucasians (II vs. ID+DD: OR = 1.43, 95% CI = 1.02-2.00, I vs. D: OR = 1.23, 95% CI 1.01-1.49). Conclusion: ACE I/D polymorphism is associated with the cancer risk in Caucasians.

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