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 language | English (US) |
|---|---|
| Pages (from-to) | 996-1001 |
| Number of pages | 6 |
| Journal | American Journal of Veterinary Research |
| Volume | 66 |
| Issue number | 6 |
| DOIs | |
| State | Published - Jun 2005 |
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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 journal › Article
}
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 -