1.The levels of transforming growth factor-β1 mRNA and estrogen receptor βwt mRNA expression on peripheral blood monocytes of patients with chronic fatigue syndrome
Haiying ZHANG ; Zhandong LIU ; Chaojun HU ; Yang ZHANG ; Xue FENG ; Shumeng BAO ; Yongbo ZHANG ; Dexin WANG ; Yongzhe LI
Chinese Journal of Laboratory Medicine 2009;32(7):745-748
Objective To detect the expression of TGF-β1 mRNA and ERβwt mRNA in peripheral blood monoanclear cells (PBMCs) in patients with chronic fatigue syndrome (CFS), and their relationship with pathogenesis of CFS. Methods Fluorescence quantitative RT-PCR (FQ-RT-PCR) was used to examine TGF-β1 mRNA and ERβwt mRNA expression of peripheral blood monocytes in 63 cases with CFS,50 cases with other diseases, and 50 healthy controls. The gene expression levels were calculated with the formula △Ct=Ct(target gene) - Ct(internal control). Results The mean TGF-β1 mRNA expression of CFS patients (△Ct = 3.27 ± 0. 58) was higher than that of disease controls (△Ct = 4. 54 ± 1.05, t = 8. 11, P <0.01) and that of healthy controls (△Ct = 4. 37 ± 1.00, t = 7. 02, P < 0. 01). The mean ERβwt mRNA expression of CFS patients (△Ct =9. 34 ±0. 92) was lower than that of disease controls(△Ct =7.12±0. 47, t = 15.44 ,P < 0. 01) and that of healthy controls(△Ct = 7. 10 ±0. 48, t = 15.47, P < 0. 01). Conclusions The TGF-β1 mRNA and ER βwt mRNA expression levels of PBMCs are siguificantly elevated in patients with CFS. It may be implicated in the pathogenesis of CSF.
2.Correlation of gastroesophageal reflux and asthma-like pathophysiological changes
Xi-Zhe YUAN ; Yongbo BAO ; Huan-Sheng XU ; Jin-Zi LI
Chinese Journal of Applied Clinical Pediatrics 2013;28(16):1235-1239
Objective To investigate whether gastroesophageal reflux can cause asthma-like pathophysiological changes and its mechanism.Methods Sixty BALB/c mice were randomly divided into 4 groups:group A was gastroesophageal reflux control group,group B was asthma control group,group C was gastroesophageal reflux group,and group D was asthmatic group.The asthmatic models were replicated with ovalbumin(OVA) and aluminum hydroxide,and gastroesophageal reflux models were replicated with hydrochloric acid solution pepsin.After the last inhaling ovalbumin and slow perfusion,the airway pressure was detected,and eosinophil (EOS) and neutrophil granulocyte in bronchial lavage fluid were counted.The flow cytometer was used to determinate IL-4,IFN-γ,and Th1/Th2 ratio changes of spleen cells;Lung tissue and esophagus sections were stained with HE,and pathological changes of lung tissue and esophagus were observed.Results In group C and group D,the airway hyper-responsiveness was significantly increased compared with group A and group B,and the differences were statistically significant (all P < 0.05).In group C and group D,IL-4were significantly increased,while IFN-γand Thl/Th2 ratio were significantly decreased than that in the group A and B group,the differences were statistically significant (all P < 0.05).EOS of group C and group D accounted for a high percentage of total cells and they were significantly higher than that in group A and group B,and the differences were statistically significant (all P < 0.05).Through lung tissue biopsy,in group C and group D,bronchial lumen deformation,infiltration of inflammatory cells around the wall,basement membrane thickening,inflammatory cell infiltration around the wall,peripheral vascular edema,enlarging alveolar cavity,alveolar wall thinning,fracture,part of alveolar fusion into bullace of lung,could be observed.The lung pathological section showed that the endothelial cells in group A and group B were integrated and had no denaturation or necrosis,and there was no inflammation cell infiltrate around.EOS biopsy could be observed in group A and group B of lower esophagus markedly submucosal edema,submucosal inflammatory cell infiltration,and keratin hyper function,visible bacteria group A group B and group D were basic ally normal,with no pathological changes.Conclusions Gastroesophageal reflux can induce Th1/Th2 decreasing,airway hyper-responsiveness and pathophysiological changes similar to asthma.