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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.


Yang J.,Huazhong University of Science and Technology | Xiang F.,Huazhong University of Science and Technology | Xiang F.,Key Laboratory of Respiratory Diseases | Cai P.-C.,Huazhong University of Science and Technology | And 17 more authors.
American Journal of Physiology - Lung Cellular and Molecular Physiology | Year: 2016

Pleural fibrosis is defined as an excessive deposition of extracellular matrix (ECM) components that results in destruction of the normal pleural tissue architecture. It can result from diverse inflammatory conditions, especially tuberculous pleurisy. Pleural mesothelial cells (PMCs) play a pivotal role in pleural fibrosis. Calpain is a family of calcium-dependent endopeptidases, which plays an important role in ECM remodeling. However, the role of calpain in pleural fibrosis remains unknown. In the present study, we found that tuberculous pleural effusion (TPE) induced calpain activation in PMCs and that inhibition of calpain prevented TPE-induced collagen-I synthesis and cell proliferation of PMCs. Moreover, our data revealed that the levels of angiotensin (ANG)-converting enzyme (ACE) were significantly higher in pleural fluid of patients with TPE than those with malignant pleural effusion, and ACE-ANG II in TPE resulted in activation of calpain and subsequent triggering of the phosphatidylinositol 3-kinase (PI3K)/Akt/NF-κB signaling pathway in PMCs. Finally, calpain activation in PMCs and collagen depositions were confirmed in pleural biopsy specimens from patients with tuberculous pleurisy. Together, these studies demonstrated that calpain is activated by renin-angiotensin system in pleural fibrosis and mediates TPE-induced collagen-I synthesis and proliferation of PMCs via the PI3K/Akt/NF-κB signaling pathway. Calpain in PMCs might be a novel target for intervention in tuberculous pleural fibrosis. © 2016 the American Physiological Society.


Shi H.,Huazhong University of Science and Technology | Shi H.,Key Laboratory of Respiratory Diseases | Cheng D.,Huazhong University of Science and Technology | Cheng D.,Key Laboratory of Respiratory Diseases | And 8 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2015

The aim of this study was to determine whether orosomucoid1- like 3 (ORMDL3) single nucleotide polymorphisms rs7216389, rs11650680, rs12603332 are associated with susceptibility to asthma. We performed a meta-analysis by searching PubMed, EMBASE, Elsevier and Wanfang Databases. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to evaluate the strength of associations. We examined the association between the three SNPs and asthma risk in four genetic models (TT + TC vs. CC, TC vs. CC, TT vs. CC, TT vs. TC + CC). Thirteen published case-control studies involving 6462 cases and 7357 controls were included. Our meta-analysis indicated that rs7216389 was significantly associated with increased asthma risk in overall population. Subgroup analysis by age indicated significant association between the rs7216389 and asthma in children. Moreover, ORMDL3 rs11650680 was significantly associated with decreased asthma risk in dominant model (TT + TC vs. CC), and rs12603332 was significantly associated with decreased asthma risk in 3 models (TT + TC vs. CC, TC vs. CC and TT vs. CC). To Conclude, ORMDL3 rs7216389 polymorphism is associated with susceptibility to asthma. Children with variant T allele (TT or TC) and adults with TT homozygote in rs7216389 are at high risks to suffer from asthma. However, people with T allele in rs11650680 or rs12603332 are protected from asthma. © 2015, E-Century Publishing Corporation. All rights reserved.


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.


Cheng D.,Huazhong University of Science and Technology | Cheng D.,Key Laboratory of Respiratory Diseases | Shi H.,Huazhong University of Science and Technology | Shi H.,Key Laboratory of Respiratory Diseases | And 6 more authors.
Diagnostic Pathology | Year: 2014

Objectives: RAD51 gene plays an important role in the pathogenesis of squamous cell carcinoma of the head and neck (SCCHN), colorectal cancer, ovarian cancer and acute leukaemia. A number of studies assessed the association between RAD51 135G/C polymorphism and the risk of these cancers in different population. However, the results have been inconclusive. We performed a systematic meta-analysis to evaluate the association between RAD51 135G/C polymorphism and the risk of these four types of cancer.Methods: Pubmed, Cochrane library and Chinese Biomedical Literature Database (CBM) were searched for case-control studies on RAD51 135G/C polymorphism and the risk of SCCHN, colorectal cancer, ovarian cancer and acute leukaemia published up to Oct 31, 2013. Odds ratios (ORs) with 95% confidence intervals (CIs) were used to assess the strength of association.Results: A total of twenty-two published studies, with 6836 cases and 8507 controls were included. Overall, no significant association was found between RAD51 135G/C polymorphism and the risk of the four types of cancers (G/G vs. C/C: OR = 0.83, 95% CI: 0.43-1.59, P = 0.57). However, there was a significant association between this polymorphism and SCCHN risk in the subgroup analysis by cancer type (G/G vs. C/C: OR = 2.46, 95% CI: 1.08-5.61, P = 0.03).Conclusion: The RAD51 135G/C polymorphism was associated with the risk of SCCHN.Virtual slides: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1383180234106945. © 2014 Cheng et al.; licensee BioMed Central Ltd.


Yi L.,Huazhong University of Science and Technology | Yi L.,Key Laboratory of Respiratory Diseases | Cheng D.,Huazhong University of Science and Technology | Cheng D.,Key Laboratory of Respiratory Diseases | And 10 more authors.
International Journal of Clinical and Experimental Medicine | Year: 2014

A 38-year-old female was found to have multiple bilateral lung nodules in a routine chest X-ray examination. Thoracoscopy was performed with biopsy of three nodules from the right lower lobe and Congo red staining showed typical amyloid pattern. Initial diagnosis of pulmonary nodular amyloidosis was made. However, one nodule in the right upper lobe enlarged as detected by follow-up CT scan. The patient underwent F-18 fluorodeoxyglucose positron emission tomography (18F-FDG-PET)/CT and a significant high FDG uptake in the largest nodule in right upper lobe was observed while the uptake was normal or mildly increased in the other nodules. Meanwhile, right hilar and mediastinal lymph nodes adenopathy was noted. Right upper lobe was resected by thoracotomy. Surprisingly, histopathological findings showed pulmonary epithelioid hemangioendothelioma (PEH) with metastasis of hilar and mediastinal lymph nodes. To our knowledge, this is the first described case of PEH coexisting with pulmonary nodular amyloidosis.

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