Background <p>A secondary <i>Pasteurella multocida</i> (<i>Pm</i>) infection following <i>Mycoplasma ovipneumoniae</i> (<i>Mo</i>) 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 <i>Mo</i>-associated secondary <i>Pm</i> infection is less understood.</p> Methods and results <p>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 <i>Pm</i> 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 <i>Pm</i>. However, <i>Mo</i> infection downregulated SRA expression and impaired AM-mediated phagocytosis of <i>Pm</i>; 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.</p> Conclusions <p>The findings of this study elucidate the role of SRA in <i>Mo</i>-induced secondary <i>Pm</i> infection and provide some support for in-depth exploration in subsequent studies.</p>

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Mycoplasma ovipneumoniae infection inhibits scavenger receptor A—mediated phagocytosis of Pasteurella multocida in alveolar macrophages

  • Guangxin Zhao,
  • Xinyan Cao,
  • Guojie Cheng,
  • Gang Wang,
  • Sun He,
  • Jinliang Sheng,
  • Yanming Sun,
  • Yanbing Zhang

摘要

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.