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

Lynelle R Johnson, Hilda E V De Cock, Jane E Sykes, Philip H Kass, David J Maggs, Christian M. Leutenegger

Research output: Contribution to journalArticle

9 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)996-1001
Number of pages6
JournalAmerican Journal of Veterinary Research
Volume66
Issue number6
DOIs
StatePublished - Jun 2005

Fingerprint

Felidae
Nose
Cats
cytokines
transcription (genetics)
inflammation
cats
Cytokines
Inflammation
Genes
tumor necrosis factors
interleukin-12
interferons
chemokines
genes
Interleukin-12
interleukin-10
Interleukin-16
Chemokines
interleukin-6

ASJC Scopus subject areas

  • veterinary(all)

Cite this

Cytokine gene transcription in feline nasal tissue with histologic evidence of inflammation. / Johnson, Lynelle R; De Cock, Hilda E V; Sykes, Jane E; Kass, Philip H; Maggs, David J; Leutenegger, Christian M.

In: American Journal of Veterinary Research, Vol. 66, No. 6, 06.2005, p. 996-1001.

Research output: Contribution to journalArticle

@article{179054aa567c4e4285bdc5a333555d49,
title = "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]-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.",
author = "Johnson, {Lynelle R} and {De Cock}, {Hilda E V} and Sykes, {Jane E} and Kass, {Philip H} and Maggs, {David J} and Leutenegger, {Christian M.}",
year = "2005",
month = "6",
doi = "10.2460/ajvr.2005.66.996",
language = "English (US)",
volume = "66",
pages = "996--1001",
journal = "American Journal of Veterinary Research",
issn = "0002-9645",
publisher = "American Veterinary Medical Association",
number = "6",

}

TY - JOUR

T1 - Cytokine gene transcription in feline nasal tissue with histologic evidence of inflammation

AU - Johnson, Lynelle R

AU - De Cock, Hilda E V

AU - Sykes, Jane E

AU - Kass, Philip H

AU - Maggs, David J

AU - Leutenegger, Christian M.

PY - 2005/6

Y1 - 2005/6

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=21344464710&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=21344464710&partnerID=8YFLogxK

U2 - 10.2460/ajvr.2005.66.996

DO - 10.2460/ajvr.2005.66.996

M3 - Article

C2 - 16008222

AN - SCOPUS:21344464710

VL - 66

SP - 996

EP - 1001

JO - American Journal of Veterinary Research

JF - American Journal of Veterinary Research

SN - 0002-9645

IS - 6

ER -