Cytokine gene transcription in feline nasal tissue with histologic evidence of inflammation.

Abstract

OBJECTIVE: To correlate gene transcription of cytokines and chemokines with histologic inflammation in nasal biopsy specimens of cats. ANIMALS: 25 study cats and 4 specific pathogen-free cats. PROCEDURE: One nasal biopsy specimen from each cat was submitted for routine histologic evaluation; a second was submitted for evaluation by use of a quantitative real-time polymerase chain reaction analysis with a fluorogenic probe (ie, TaqMan) for detection of cytokines and chemokines (interleukin [IL]-4, IL-5, IL-6, IL-10, IL-12 p40, IL-16, IL-18, interferon [IFN]I-gamma, tumor necrosis factor [TNF]-alpha, and the regulated on activation normal T cell expressed and secreted [RANTES] protein). Specimens were grouped histologically by degree of inflammation (none, mild, moderate, or severe). Linearized TaqMan signals for each gene were compared among histologic groups. RESULTS: Nasal biopsy specimens from specific pathogen-free cats were histologically normal, and cytokine transcription was low in these samples. As nasal inflammation in study cats worsened from absent (n = 3) to mild (4) to moderate (8) or severe (10), progressively and significantly increasing transcription of IL-6, IL-10, IL-12 p40, IFN-gamma, TNF-alpha, and the RANTES protein was detected. Transcription of IL-4, IL-5, IL-16, and IL-18 did not correlate with worsened histologic inflammation. CONCLUSIONS AND CLINICAL RELEVANCE: Transcription of specific cytokines and chemokines in nasal tissue of cats progressively increased with severity of histologic evidence of inflammation, and IL-6, IL-10, IL-12 p40, IFN-gamma, TNF-alpha, and the RANTES protein were markers of inflammation. Our data suggest that the nasal cavity of cats is biased toward a Th1 cytokine profile that is augmented by inflammation.