Feline infectious peritonitis (FIP) is an almost invariably fatal feline 
coronavirus (FCoV)-induced disease thought to arise from a combination of viral 
mutations and an overexuberant immune response. Natural initial enteric FCoV 
infection may remain subclinical, or result in mild enteric signs or the 
development of FIP; cats may also carry the virus systemically with no adverse 
effect. This study screened mesenteric lymph nodes (MLNs), the presumed first 
site of FCoV spread from the intestine regardless of viraemia, for changes in 
the transcription of a panel of innate immune response mediators in response to 
systemic FCoV infection and with FIP, aiming to identify key pathways triggered 
by FCoV. Cats with and without FIP, the latter with and without FCoV infection 
in the MLN, were compared. Higher expression levels in FIP were found for 
toll-like receptors (TLRs) 2, 4 and 8. These are part of the first line of 
defence and suggest a response to both viral structural proteins and viral 
nucleic acid. Expression of genes encoding inflammatory cytokines and 
chemokines, including interleukin (IL)-1β, IL-6, IL-15, tumour necrosis factor 
(TNF)-α, CXCL10, CCL8, interferon (IFN)-α, IFN-β and IFN-γ, was higher in cats 
with FIP, consistent with inflammatory pathway activation. Expression of genes 
encoding transcription factors STAT1 and 2, regulating signalling pathways, 
particularly of the interferons, was also higher. Among cats without FIP, there 
were few differences between virus-positive and virus-negative MLNs; however, 
TLR9 and STAT2 expression were higher with infection, suggesting a direct viral 
effect. The study provides evidence for TLR involvement in the response to FCoV. 
This could open up new avenues for therapeutic approaches.