We report that: (i) plasma from C. difficile-infected mice was sufficient to upregulate neutrophil CXCR2 expression; (ii) CDI-induced CXCR2 was upregulated only on a sub-population of neutrophils: CD11bhi neutrophils; and (iii) Interleukin (IL)-1β was a key driver of CDI-induced neutrophil CXCR2 expression and subsequent colonic neutrophil accumulation. The gene discussed is IL1B; the disease is clostridium difficile infection.