Lymphocyte chemokine expression and its effect on peripheral blood CD4+ CD8+ T-cell subsets in patients with chronic obstructive pulmonary disease
Author(s): Zhuo Songming, Li Na, Xun Anying, Liang Wenmei, Zheng Yi
Pages: 12-16
Year: 2015 Issue: 1
Journal: International Journal of Respiration
Keyword: Chronic obstructive pulmonary disease; Lymphocyte chemokine; T-lymphocyte subset; Apoptosis; Interleukin-2;
Abstract: Objective In this study,we sought to investigate the relevance of lymphocyte chemokine (lymphotactin,XCL1) expression in patients with chronic obstructive pulmonary disease (COPD) and to analyze the effects of XCL1 expression on CD4+ CD8+ T-cell subsets and related inflammatory factors.Methods Thirteen patients with COPD [acute exacerbation (AE) and stable phase (SP)] and 13 healthy individuals were included in the study.Peripheral blood T lymphocytes were isolated aud cultured.After XCL1 intervention,subsets of peripheral blood CD4+ CD8+ T lymphocytes and expression of Fas and FasL were detected by flow cytometry.XCL1 and interleukin (IL)-2 expression in sera and cell culture supernatants were detected by enzyme linked immunosorbent assay.Results XCL1 expression in the peripheral blood of patients with COPD (both AE and SP) was higher than that in healthy patients.Additionally,XCL1 expression was higher during AE than during SP.Analysis of T cells from the culture medium of COPD patients revealed that CD4 +-Fas,CD4+-FasL,CD8~ Fas,and CD8+-FasL subsets increased,while the CD4+ CD8+ subset decreased following XCL1 intervention.Moreover,IL-2 expression decreased,and XCL1 expression,as well as CD4+-Fas,CD4+-FasL,CD8+-Fas,and CD8+-FasL subsets,were positively correlated with IL-2 expression,while the CD4+ CD8+ subset was negatively correlated.Conclusions XCL1 involved in the inflammatory process of COPD,which through by increasing the expression of Fas,FasL,and resulted in CD4 + T,CD8 + T cells apoptosis increased,CD4 + T/CD8+ T decreased,caused the imbalance of the proportion of CD4+/CD8+.XCL1 also decreased the level of IL-2,thereby representing an important molecular player in the persistent inflammation observed in COPD.
Pages: 12-16
Year: 2015 Issue: 1
Journal: International Journal of Respiration
Keyword: Chronic obstructive pulmonary disease; Lymphocyte chemokine; T-lymphocyte subset; Apoptosis; Interleukin-2;
Abstract: Objective In this study,we sought to investigate the relevance of lymphocyte chemokine (lymphotactin,XCL1) expression in patients with chronic obstructive pulmonary disease (COPD) and to analyze the effects of XCL1 expression on CD4+ CD8+ T-cell subsets and related inflammatory factors.Methods Thirteen patients with COPD [acute exacerbation (AE) and stable phase (SP)] and 13 healthy individuals were included in the study.Peripheral blood T lymphocytes were isolated aud cultured.After XCL1 intervention,subsets of peripheral blood CD4+ CD8+ T lymphocytes and expression of Fas and FasL were detected by flow cytometry.XCL1 and interleukin (IL)-2 expression in sera and cell culture supernatants were detected by enzyme linked immunosorbent assay.Results XCL1 expression in the peripheral blood of patients with COPD (both AE and SP) was higher than that in healthy patients.Additionally,XCL1 expression was higher during AE than during SP.Analysis of T cells from the culture medium of COPD patients revealed that CD4 +-Fas,CD4+-FasL,CD8~ Fas,and CD8+-FasL subsets increased,while the CD4+ CD8+ subset decreased following XCL1 intervention.Moreover,IL-2 expression decreased,and XCL1 expression,as well as CD4+-Fas,CD4+-FasL,CD8+-Fas,and CD8+-FasL subsets,were positively correlated with IL-2 expression,while the CD4+ CD8+ subset was negatively correlated.Conclusions XCL1 involved in the inflammatory process of COPD,which through by increasing the expression of Fas,FasL,and resulted in CD4 + T,CD8 + T cells apoptosis increased,CD4 + T/CD8+ T decreased,caused the imbalance of the proportion of CD4+/CD8+.XCL1 also decreased the level of IL-2,thereby representing an important molecular player in the persistent inflammation observed in COPD.
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