Complement C1q inhibits the immune escape of mycobacterium tuberculosis associated with macrophage inflammation levels and glycolytic activation

Background The pathogenic mechanism of mycobacterium tuberculosis (Mtb) is complex, and the immune mechanism of the host against Mtb infection and the escape mechanism of Mtb are not fully understood. This study aimed to explore the mechanisms underlying complement C1q and Mtb immune escape. Methods Functional experiments, using RAW264.7 cells as the focus cell line and applying CCK-8, western blotting, qRT-PCR, and flow cytometry, were carried out to uncover the exact role of C1q in macrophages, glycolytic activation, immune escape, and Mtb. Results C1q promoted the proliferation of RAW264.7, suppressed cell apoptosis, and regulated the secretion of M1/M2 type molecular markers in RAW264.7 cells. Moreover, C1q induced glycolytic activation in macrophages, and the immune escape of Mtb in the macrophages was accompanied by the activation of glycolysis. Conclusion Complement C1q inhibited the immune escape of Mtb associated with macrophage inflammation and glycolytic activation.