Data from: CCL28 modulates neutrophil responses during infection with mucosal pathogens

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 in the gut of mice infected with Salmonella and in
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 varied between the two infections: 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 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 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.