The mouse Pactolus gene is an evolutionary paralogue to the CD18/beta2 integrin subunit and is preferentially expressed by neutrophils. When first identified, it was assumed Pactolus would function as an adhesion receptor similar to other beta integrin subunits. The analysis of mice genetically deficient in Pactolus, however, did not define any lesion in neutrophil migration, adhesion or phagocytosis. Therefore a wider analysis of the Pactolus deficiency was initiated using transcriptional profiling during an inflammatory insult. This screen identified a single transcript, CXCL13, that was elevated in cells from a peritoneal lavage of the wild type animal compared to the Pactolus-deficient animal. Our analyses confirmed resident macrophages as being responsible for the chemokine using intracellular CXCL13 staining and additional cell markers to phenotypically characterize such cells. The resident CXCL13-expressing cells (which do not express Pactolus) are functionally distinct from the macrophages recruited into the peritoneal cavity following the inflammatory stimulation since the recruited macrophages do not express detectable levels of the chemokine. The numbers and expression patterns of these resident CXCL13-expressing cells do not vary in naïve animals of wild type or Pactolus-deficient origin. Additionally, Pactolus-deficient neutrophils do not preferentially kill (compared to wild type) CXC13-expressing macrophages. These data suggest that during an inflammatory response, Pactolus may help retain CXCL13-expressing cells within the peritoneal environment.