
CCL28 は粘膜感染症の際に好中球の動員と活性化を促進し、病原体排除と組織損傷のバランスを調節する重要な因子である。


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The chemokine CCL28 is highly expressed in mucosal tissues, but its role during infection is not well understood. Here we show that CCL28 promotes neutrophil accumulation to the gut of mice infected with Salmonella and to the lung of mice infected with Acinetobacter . Neutrophils isolated from the infected mucosa expressed the CCL28 receptors CCR3 and, to a lesser extent, CCR10, on their surface. The functional consequences of CCL28 deficiency were different between the two infections, as Ccl28 -/- mice were highly susceptible to Salmonella gut infection, but highly resistant to otherwise lethal Acinetobacter lung infection. In vitro , unstimulated neutrophils harbored pre-formed intracellular CCR3 that was rapidly mobilized to the cell surface following phagocytosis or inflammatory stimuli. Moreover, CCL28 stimulation enhanced neutrophil antimicrobial activity, production of reactive oxygen species, and formation of extracellular traps, all processes that were largely dependent on CCR3. Consistent with the different outcomes in the two infection models, neutrophil stimulation with CCL28 boosted the killing of Salmonella but not of Acinetobacter . CCL28 thus plays a critical role in the immune response to mucosal pathogens by increasing neutrophil accumulation and activation, which can enhance pathogen clearance but also exacerbate disease depending on the mucosal site and the infectious agent.

### Competing Interest Statement

The authors have declared no competing interest.

CCL28 modulates neutrophil responses during infection with mucosal pathogens

サルモネラ感染症とアシネトバクター肺炎における-ccl28-の役割-好中球の動員と活性化を通じた粘膜免疫応答の調節


サルモネラ感染症とアシネトバクター肺炎における CCL28 の役割 - 好中球の動員と活性化を通じた粘膜免疫応答の調節
