[Effect of 2 Gene Silencing on Mouse Macrophage Resistance Against Infection via TLR Pathway].

OBJECTIVE

To investigate the effect of silencing protein phosphatase 2cm ( 2) gene on the expression of inflammatory factors in macrophages infected with ( . ) and the mechanisms involved.

METHODS

The effects of 2 knockdown on inflammatory factors, proliferation, apoptosis, and Toll-like receptor (TLR) signaling were analyzed in RAW 264.7 cells, a murine macrophage cell line, transfected with adenovirus (Ad). The cells were divided into four groups, including Ad-Ctrl group, Ad- 2 group, Ad-Ctrl+ . group and Ad- 2+ . group. Cell transfection was achieved by separately introducing control adenovirus (Ad-Ctrl) or adenovirus targeting the 2 gene (Ad- 2) and inflammation or the absence of inflammation was induced by applying or not applying . . The expression of tumor necrosis factor-alpha ( ), interleukin-1β ( -1 ), 2, 4, Toll-like receptor adaptor protein ( ) and myeloid differentiation factor 88 ( 88) was determined by real-time fluorescent quantitative polymerase chain reaction (RT-qPCR). PP2Cm protein expression was determined by Western blot. Cell proliferation was determined by cell counting kit-8 (CCK-8) assay and cell apoptosis was measured by flow cytometry.

RESULTS

The expression of 2gene and PP2Cm protein was downregulated in the Ad- 2 group when compared to the Ad-Ctrl group, with the diference showing statistical significance ( <0.05). When compared to those of the Ad-Ctrl+ . group, macrophages in the Ad- 2+ . group showed significantly increase in the - and -1 gene levels ( <0.01). Furthermore, the Ad- 2 group demonstrated elevated gene expression levels of 2, 4, and 88 in macrophages when compared to the Ad-Ctrl group, with the difference showing statistical significance ( <0.05). There were no statistically significant differences in cell apoptosis and proliferation between the Ad-Ctrl and Ad- 2 groups.

CONCLUSIONS

Silencing 2 gene promotes the inflammatory response of macrophages to . infection. Moreover, the TLR pathway plays an important role in the inflammatory activation of macrophages.