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CCL28 increases the production of reactive oxygen species during Salmonella enterica serovar Typhimurium infection

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Abstract

The mucosal chemokine CCL28 plays a protective role during Salmonella infection by mechanisms that are not well understood. Using Ccl28-/- mice, our previous studies determined that CCL28 promotes the recruitment of neutrophils during Salmonella enterica serovar Typhimurium (STm) infection and enhances the survival of wild-type (WT) mice. Here we sought to investigate whether the CCL28 receptors CCR3 and CCR10 are expressed in neutrophils and whether their activation by CCL28 promotes neutrophil function. First, neutrophils were infected with STm in order to determine changes in surface and intracellular expression of CCR3 and CCR10. Using flow cytometry, we observed that there is higher expression of intracellular and surface CCR3 when compared to CCR10 during STm infection. Furthermore, surface CCR3 expression increased after infection. The next step was to determine the mechanism by which CCL28 promotes survival of WT mice during STm infection. As neutrophils produce reactive oxygen species (ROS) as a form of defense during infection, we tested whether neutrophil ROS production would be increased in the presence of CCL28 during STm infection. Using flow cytometry, we discovered that in the presence of CCL28, neutrophil ROS production is increased during STm infection. However, when blocking CCR3 with a neutralizing antibody, neutrophil ROS production decreases. Thus, we conclude that ROS production in neutrophils stimulated with CCL28 during STm infection is primarily facilitated via CCR3.

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This item is under embargo until January 11, 2024.