title: [Effects of different cytokines on proliferation and apoptosis of pleural mesothelial cells in human Mycobacterium tuberculosis infection].
abstract: OBJECTIVE
  To investigate the effects of different cytokines (IL-22, IL-17, IFN-γ) on proliferation and apoptosis of human pleural mesothelial cells (PMC) during Mycobacterium tuberculosis infection.
  
  
  METHODS
  The expressions of IL-22R, IL-17R and IFN-γR1 on PMC purified from tuberculous pleural effusion (TPE) were determined by flow cytometry. The effects of one or more of IL-22, IL-17, and IFN-γ on Ki-67 expression and apoptosis of PMC were explored. Ki-67 expression of PMC under the conditions of the absence or presence of exogenous TPE and with a combination of control IgG, or anti-IL-22, -IL-17 or -IFN-γ mAbs were determined.
  
  
  RESULTS
  (1) During Mycobacterium tuberculosis infection, IL-22R, IL-17R and IFN-γR1 were highly expressed on the surface of PMC [(86.2 ± 2.9)%, (41.5 ± 4.4)% and (64.9 ± 5.8)% respectively]. (2) In group IL-22 + IL-17, the percentage of Ki-67(+)PMC was (31.5 ± 2.0) % and (26.1 ± 2.4) % respectively, which were both higher than that in the medium group [ (14.6 ± 0.7)%] (q = 6.8 and 4.9, respectively, both P < 0.05). In group IFN-γ, the percentage of Ki-67(+)PMC was (5.2 ± 1.2) %, which was lower than that in the medium group (q = 5.0, P < 0.05). In group IFN-γ+IL-22 and IFN-γ+IL-17, the percentages of Ki-67(+)PMC were (23.4 ± 1.7)% and (21.8 ± 3.8)% respectively, which were both higher than that in group IFN-γ (q = 7.3 and 6.7, respectively, both P < 0.05). In group TPE and TPE+IgG, the percentages of Ki-67(+)PMC were (63 ± 9) % and (63 ± 11) % respectively, which were both higher than that in the medium group (q = 19.6 and 19.7, respectively, both P < 0.05). In group TPE+ anti-IFN-γ mAb, the percentage of Ki-67(+)PMC was (82 ± 4) %, which was even higher than that in group TPE+IgG (q = 7.5,P < 0.05) . In group TPE + anti-IL-22 mAb, the percentage of Ki-67(+)PMC was (34 ± 3) %, which was lower than that in group TPE+IgG (q = 11.8, P < 0.05). In group TPE + anti-IL-17 mAb, the percentage of Ki-67(+)PMC was (58 ± 5) %, which showed no significant difference compared to that in group TPE+IgG (q = 2.1, P > 0.05). (3) The percentage of apoptotic PMC in group IFN-γ was (19.3 ± 1.1)%, which was higher than that in the medium group[ (4.3 ± 0.6)%] (q = 33.4,P < 0.05) . The percentage of apoptotic PMC in group IL-22 + IL-17 was (3.8 ± 0.6)% and (5.7 ± 0.8)% respectively, which had no significant difference compared to that in the medium group (q = 1.3 and 3.0, respectively, both P > 0.05). The percentage of apoptotic PMC in group IFN-γ + IL-22 and IFN-γ+ IL-17 were (6.5 ± 0.7) % and (8.7 ± 1.7)% respectively, which were both lower than that in group IFN-γ (q = 28.5 and 23.6, respectively, both P < 0.05).
  
  
  CONCLUSIONS
  During Mycobacterium tuberculosis infection, IFN-γ inhibited PMC proliferation and contributed to apoptosis, while IL-22 and IL-17 promoted PMC proliferation without influencing PMC apoptosis and succeeded in reversing the effect induced by IFN-γ.
authors.affiliation: Department of Respiratory and Critical Care Medicine, Key Laboratory of Pulmonary Diseases of Health Ministry, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
authors.forename: Liang
authors.initials: L
authors.lastname: Xiong
authors.forename: Fei
authors.initials: F
authors.lastname: Xiang
authors.forename: Qiong
authors.initials: Q
authors.lastname: Zhou
authors.forename: Jian-chu
authors.initials: JC
authors.lastname: Zhang
mesh_terms: D017209:Apoptosis / Q000187:drug effects; D049109:Cell Proliferation; D002478:Cells, Cultured; D016207:Cytokines / Q000378:metabolism*; D004847:Epithelial Cells / Q000166:cytology* / Q000378:metabolism; D005260:Female; D005434:Flow Cytometry; D006801:Humans; D007371:Interferon-gamma / Q000378:metabolism; D020381:Interleukin-17 / Q000378:metabolism; D007378:Interleukins / Q000378:metabolism; D008297:Male; D010994:Pleura / Q000378:metabolism / Q000473:pathology; D010996:Pleural Effusion / Q000378:metabolism*; D018123:Receptors, Interleukin / Q000378:metabolism; D014396:Tuberculosis, Pleural / Q000378:metabolism* / Q000473:pathology; D000097043:Interleukin-22
chemical_list: D016207:Cytokines; D007371:Interferon-gamma; D020381:Interleukin-17; D007378:Interleukins; D018123:Receptors, Interleukin; D000097043:Interleukin-22