CCL28 modulates neutrophil responses during infection with mucosal pathogens

Area of Science:

• Immunology
• Microbiology
• Infectious Diseases

Background:

• The chemokine CCL28 is prevalent in mucosal tissues, yet its function in host defense against pathogens remains unclear.
• Understanding CCL28's role is crucial for developing strategies against mucosal infections.

Purpose of the Study:

• To investigate the role of chemokine CCL28 in host defense against bacterial infections at mucosal sites.
• To elucidate the mechanisms by which CCL28 influences neutrophil function and impacts infection outcomes.

Main Methods:

• Utilized mouse models of *Salmonella* gut and *Acinetobacter* lung infections.
• Analyzed neutrophil recruitment, receptor expression (CCR3, CCR10), and functional responses.
• Assessed infection severity and pathogen clearance in wild-type and *Ccl28*-deficient mice.

Main Results:

• CCL28 promoted neutrophil accumulation in both gut and lung infections.
• *Ccl28*-deficient mice showed increased susceptibility to *Salmonella* but resistance to *Acinetobacter*.
• CCL28 enhanced neutrophil antimicrobial activity and extracellular trap formation, primarily via CCR3.

Conclusions:

• CCL28 plays a dual role in mucosal immunity, enhancing neutrophil responses that can be beneficial or detrimental depending on the context.
• CCL28-mediated neutrophil activation is critical for controlling *Salmonella* but not *Acinetobacter* infections.
• Targeting CCL28 or its receptors may offer therapeutic avenues for managing mucosal infections.