title: The expression of Foxp3 and ROR gamma t in lung tissues from normal smokers and chronic obstructive pulmonary disease patients.
abstract: Foxp3- and ROR gamma t-expressing cells are involved in acquired immune responses. The change in Foxp3 and ROR gamma t expression in lung tissue and their role in emphysema has not been studied for COPD patients and normal smokers. In the present study, Foxp3 and ROR gamma t were assessed using real-time quantitative polymerase chain reaction and western blotting, and the expression and distribution of Foxp3, IL-17, IL-23R and CCR6 were measured by immunohistochemistry in peripheral lung tissue (10 smokers with COPD, 10 smokers and 10 nonsmokers with normal lung function). Foxp3 expression was lower and ROR gamma t expression was higher in COPD patients when compared with smokers and nonsmokers (all P values were less than 0.001). The ratios of Foxp3/ROR gamma t mRNA and protein were positively correlated to FEV1%pred and negatively correlated to the mean alveoli area. Foxp3(+) cell numbers were decreased, while the number of IL-17(+) cells, IL-23R(+) cells and CCR6(+) cells were increased in the lung alveolar walls of COPD patients compared with normal smokers and nonsmokers (all P values were less than 0.001). The IL-17(+) cell numbers were positively correlated to both CCR6(+) and IL-23R(+) cells. Our data show a decreased Foxp3 expression and an increased ROR gamma t expression in COPD patients and normal smokers that parallels the aggravation of the disease. The IL-17(+)-cell-related cytokines receptors CCR6 and IL-23R had an association with the mechanism of IL-17(+) cell number increasing, which will provide a new immuno-therapeutic target for COPD.
authors.affiliation: Department of Respiratory Medicine, the First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China. emilyyuanchu@163.com
authors.forename: Shuyuan
authors.initials: S
authors.lastname: Chu
authors.forename: Xiaoning
authors.initials: X
authors.lastname: Zhong
authors.forename: Jianquan
authors.initials: J
authors.lastname: Zhang
authors.forename: Qifang
authors.initials: Q
authors.lastname: Lao
authors.forename: Zhiyi
authors.initials: Z
authors.lastname: He
authors.forename: Jing
authors.initials: J
authors.lastname: Bai
mesh_terms: D015153:Blotting, Western; D005260:Female; D051858:Forkhead Transcription Factors / Q000096:biosynthesis* / Q000235:genetics; D015870:Gene Expression; D006801:Humans; D020381:Interleukin-17 / Q000096:biosynthesis; D008168:Lung / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000096:biosynthesis* / Q000235:genetics; D029424:Pulmonary Disease, Chronic Obstructive / Q000235:genetics / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D060888:Real-Time Polymerase Chain Reaction; D054399:Receptors, CCR6 / Q000096:biosynthesis; D018123:Receptors, Interleukin / Q000096:biosynthesis; D012720:Severity of Illness Index; D012907:Smoking / Q000235:genetics / Q000276:immunology / Q000378:metabolism* / Q000473:pathology
chemical_list: C106311:CCR6 protein, human; C418974:FOXP3 protein, human; D051858:Forkhead Transcription Factors; C515500:IL23R protein, human; D020381:Interleukin-17; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D012333:RNA, Messenger; D054399:Receptors, CCR6; D018123:Receptors, Interleukin