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<p>Recruitment of Ly6C<sup>hi</sup> monocytes to infection sites critically contributes to the clearance of microbial pathogens. However, the mechanism regulating their migration from the peripheral blood to the infected sites remains unresolved. In this study, we demonstrate that G protein-coupled receptor GPR35 is required for the entry of circulating Ly6C<sup>hi</sup> monocytes into the sites of <i>Listeria monocytogenes</i> infection. <i>Gpr35</i><sup>−/−</sup> mice showed a decrease in Ly6C<sup>hi</sup> monocyte recruitment to the cecum and colon after oral administration of <i>L. monocytogenes</i>. They also exhibited a reduction in Ly6C<sup>hi</sup> monocytes in the liver and spleen upon intravenous infection. Mechanistically, GPR35 signaling enhanced Mac-1- and LFA-1-dependent Ly6C<sup>hi</sup> monocyte adhesion to ICAM-1, and GPR35-dependent integrin activation was important for their in vivo recruitment to infected sites. A potential GPR35-reactive metabolite, lysophosphatidic acid, accumulated around the bacterial foci near to the blood vessels. In addition, the GPR35 signal induced TNF-α production by Ly6C<sup>hi</sup> Sca-1<sup>+</sup> monocytes and restricted the bacterial burden of <i>L. monocytogenes</i>. Collectively, GPR35-mediated signaling provides the molecular cue for elimination of <i>L. monocytogenes</i> by recruiting circulating Ly6C<sup>hi</sup> monocytes to the infected sites where they produce TNF-α.</p>

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GPR35 mediates monocyte recruitment to the sites of Listeria monocytogenes infection

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月2日

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  • Yo Okamura,
  • Katsuhiro Nakanishi,
  • Ryotaro Inada,
  • Rae Maeda,
  • Kazuki Maeshima,
  • Misato Mizutani,
  • Wakana Ohashi,
  • Masahito Ikawa,
  • Yuki Sugiura,
  • Kiyoshi Takeda,
  • Eiji Umemoto

摘要

Recruitment of Ly6Chi monocytes to infection sites critically contributes to the clearance of microbial pathogens. However, the mechanism regulating their migration from the peripheral blood to the infected sites remains unresolved. In this study, we demonstrate that G protein-coupled receptor GPR35 is required for the entry of circulating Ly6Chi monocytes into the sites of Listeria monocytogenes infection. Gpr35−/− mice showed a decrease in Ly6Chi monocyte recruitment to the cecum and colon after oral administration of L. monocytogenes. They also exhibited a reduction in Ly6Chi monocytes in the liver and spleen upon intravenous infection. Mechanistically, GPR35 signaling enhanced Mac-1- and LFA-1-dependent Ly6Chi monocyte adhesion to ICAM-1, and GPR35-dependent integrin activation was important for their in vivo recruitment to infected sites. A potential GPR35-reactive metabolite, lysophosphatidic acid, accumulated around the bacterial foci near to the blood vessels. In addition, the GPR35 signal induced TNF-α production by Ly6Chi Sca-1+ monocytes and restricted the bacterial burden of L. monocytogenes. Collectively, GPR35-mediated signaling provides the molecular cue for elimination of L. monocytogenes by recruiting circulating Ly6Chi monocytes to the infected sites where they produce TNF-α.