[Signaling pathway of M2-type polarization induced by Mycobacterium tuberculosis-specific peptide E7 in monocyte-macrophages].

Objective To explore the signal pathway of M2-type polarization induced by Mycobacterium tuberculosis (MTB)-specific peptide E7. Methods Monocyte-macrophages were divided into blank control group, M1 positive stimulus group [co-stimulated with lipopolysaccharide and gamma interferon (IFN-γ)], M2 positive group(co-stimulated with IL-4 and IL-13), and E7 experimental group (with MTB-specificity polypeptide E7 stimulated). The expression of M1 type markers CD16, IL-6, TNF-α and M2 type markers CD163, CD206, IL-10 were detected at 12, 18, 24 and 36 h. Furthermore, peroxisome proliferators-activated receptors-γ (PPAR-γ) blocker was used in the blank control group, M2-positive stimulus group and E7 experimental stimulus group. T test was used to compare the expression of PPAR-γ and CD163 before and after the addition of blockers. Results Compared with the positive control group and the blank control group, the expression of TNF-α in the E7 experimental group gradually reached the peak when macrophages were stimulated for 18 h(the relative expression was 20.02), and then the expression of TNF-α gradually decreased and the expression of CD163 increased. The expression of CD163 peaked at 24 h (the relative expression was 2.44). After adding the inhibitor, the expression of PPAR-γ in E7 stimulation group was lower than before blocking (before blocking 0.94±0.06, after blocking 0.69±0.09, P=0.028). CD163 expression level was significantly lower than that before blocking (before blocking 3.95±0.61, after blocking 2.87±0.20, P=0.047). Conclusion The MTB-specific peptide E7 induced differentiation of macrophages into M2 type, a process that may be involving PPAR-γ in just another kinase-signal transducer and activator of transcription pathway. Key words: Mycobacterium tuberculosis; Peptides; Macrophages