Effects of TLR2 on theinflammatory response and phagocytosis and killing of macrophages after Corynebacterium pseudotuberculosis infection
10.16303/j.cnki.1005-4545.2025.06.14
- VernacularTitle:TLR2对伪结核棒状杆菌感染巨噬细胞炎性反应和吞噬杀伤的影响
- Author:
Shaojie QIN
1
;
Zhiguo GONG
;
Bo LIU
;
Shuangyi ZHANG
;
Jiamin ZHAO
;
Rentana WU
;
Yusheng WANG
;
Jun JIA
;
Wei MAO
Author Information
1. 内蒙古农业大学兽医学院,内蒙古呼和浩特 010018
- Publication Type:Journal Article
- Keywords:
Corynebacterium pseudotuberculosis;
transcriptome sequencing;
macrophage;
inflamma-tory response;
phagocytosis
- From:
Chinese Journal of Veterinary Science
2025;45(6):1210-1217
- CountryChina
- Language:Chinese
-
Abstract:
Corynebacterium pseudotuberculosis(C.pseudotuberculosis)is a group of intracellular Gram-positive bacteria that can cause zoonotic diseases.This study investigated the mechanisms of inflammatory mediator secretion and the phagocytic and bactericidal functions of mouse peritoneal macrophages following C.pseudotuberculosis infection.Initially,transcriptomic sequencing was em-ployed to identify genes critical for C.pseudotuberculosis infection in macrophages.Subsequently,gene knockout mice were utilized to assess the impact of these key genes on inflammatory media-tor secretion,activation of inflammatory signaling pathways,and the phagocytic and bactericidal functions of macrophages infected with C.pseudotuberculosis.Techniques such as ELISA,Western blot,and immunofluorescence were employed in this analysis.Further,transcriptomic sequencing was conducted to identify key downstream genes.Following C.pseudotuberculosis infection,GO enrichment analysis was performed,and TLR2 was identified as the focal point of the study.Perito-neal macrophages from C57BL/6J and TLR2 knockout(TLR2-/-)mice were infected with C.pseudotuberculosis.ELISA results revealed that the levels of TNF-α,IL-1β,and IL-10 were signifi-cantly downregulated in TLR2-/-macrophages compared to C57BL/6J macrophages post-infec-tion.Western blot demonstrated that the absence of TLR2 led to a marked decrease in M APK(p38 and ERK)signaling pathway phosphorylation following C.pseudotuberculosis infection.Immuno-fluorescence results indicated that the phagocytic rate of TLR2-/-macrophages was significantly higher than that of C57BL/6J macrophages after infection.Subsequently,transcriptomic analysis of C57BL/6J and TLR2-/-macrophages infected with C.pseudotuberculosis was performed,followed by GO enrichment analysis of differential genes.IL-36a,Cx3cr1,TLR1,and TLR2 were identified as key differential genes.TLR2 plays a crucial role in the inflammatory response induced by C.pseudotuberculosis infection in mice,influencing the progression of the inflammatory response and host outcomes through the secretion of inflammatory mediators,activation of signaling pathways,and modulation of phagocytic and bactericidal functions.IL-36a and Cx3cr1 were identified as key downstream factors in this process.
