Molecular biology reports · 2025
Mycoplasma ovipneumoniae infection inhibits scavenger receptor A-mediated phagocytosis of Pasteurella multocida in alveolar macrophages.
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Zhao Guangxin, Cao Xinyan, Cheng Guojie, Wang Gang, He Sun, Sheng Jinliang, Sun Yanming, Zhang Yanbing
Аннотация
BACKGROUND: A secondary Pasteurella multocida (Pm) infection following Mycoplasma ovipneumoniae (Mo) challenge in sheep results in severe respiratory disease. Scavenger receptor A (SRA) is a key phagocytic receptor on macrophages, which facilitates microbial clearance. However, the role of sheep SRA in Mo-associated secondary Pm infection is less understood.
METHODS AND RESULTS: The expression of SRA was found to be the highest in alveolar macrophages (AMs) compared with lung tissue and spleen using quantitative polymerase chain reaction. Also, SRA was expressed in various tissues of sheep. SRA overexpression significantly enhanced Pm uptake by CHO cells, whereas fucoidan (a type A scavenger receptor-specific blocker) markedly reduced bacterial phagocytosis by AMs. This indicated an essential role of sheep SRA in macrophage phagocytosis of Pm. However, Mo infection downregulated SRA expression and impaired AM-mediated phagocytosis of Pm; this effect was reversed by SRA overexpression. Furthermore, we presumed that this might be due to the inhibition of SRA expression by tumor necrosis factor-alpha and interleukin 6, thereby suppressing SRA-dependent phagocytosis.
CONCLUSIONS: The findings of this study elucidate the role of SRA in Mo-induced secondary Pm infection and provide some support for in-depth exploration in subsequent studies.
METHODS AND RESULTS: The expression of SRA was found to be the highest in alveolar macrophages (AMs) compared with lung tissue and spleen using quantitative polymerase chain reaction. Also, SRA was expressed in various tissues of sheep. SRA overexpression significantly enhanced Pm uptake by CHO cells, whereas fucoidan (a type A scavenger receptor-specific blocker) markedly reduced bacterial phagocytosis by AMs. This indicated an essential role of sheep SRA in macrophage phagocytosis of Pm. However, Mo infection downregulated SRA expression and impaired AM-mediated phagocytosis of Pm; this effect was reversed by SRA overexpression. Furthermore, we presumed that this might be due to the inhibition of SRA expression by tumor necrosis factor-alpha and interleukin 6, thereby suppressing SRA-dependent phagocytosis.
CONCLUSIONS: The findings of this study elucidate the role of SRA in Mo-induced secondary Pm infection and provide some support for in-depth exploration in subsequent studies.