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

Lynelle R. Johnson DVM, PhD1, Hilde E. V. De Cock DVM, PhD2, Jane E. Sykes BVSc, PhD3, Philip H. Kass DVM, PhD4, David J. Maggs BVSc5, and Christian M. Leutenegger Dr med vet, PhD6
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  • 1 Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA 95616.
  • | 2 Departments of Pathology, Immunology, and Microbiology, School of Veterinary Medicine, University of California, Davis, CA 95616.
  • | 3 Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA 95616.
  • | 4 Department of Population Health and Reproduction, School of Veterinary Medicine, University of California, Davis, CA 95616.
  • | 5 Department of Surgical and Radiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616.
  • | 6 Department of Medicine and Epidemiology, School of Veterinary Medicine, University of California, Davis, CA 95616.

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]-γ, tumor necrosis factor [TNF]-α, 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-γ, TNF-α, 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-γ, TNF-α, 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. (Am J Vet Res 2005;66:996–1001)

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]-γ, tumor necrosis factor [TNF]-α, 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-γ, TNF-α, 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-γ, TNF-α, 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. (Am J Vet Res 2005;66:996–1001)