Zhonghua jie he he hu xi za zhi = Zhonghua jiehe he huxi zazhi = Chinese journal of tuberculosis and respiratory diseases · 2013
[Effects of different cytokines on proliferation and apoptosis of pleural mesothelial cells in human Mycobacterium tuberculosis infection].
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Xiong Liang, Xiang Fei, Zhou Qiong, Zhang Jian-chu
Аннотация
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).
CONCLUSION: 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.
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).
CONCLUSION: 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.