duodenal biopsy specimens were collected from control cats ( n  =  21 ) and cats with ibd or dietary hypersensitivity ( n  =  13 ) , collectively referred to as inflammatory enteropathy. control cats were specific pathogenfree ( spf ) animals 24  years of age with no history or clinical signs of gi disease . these animals were part of an experimental study , and the samples included in this study were taken before the start of the experiment . duodenal biopsy specimens were collected on 2 occasions from each cat and results represent an average of these 2 time points . the cats were kept under conditions approved by the uk home office and institutional ethical committee . cats with inflammatory enteropathy had evidence of vomiting , diarrhea , weight loss , or some combination of these signs for a minimum of 2  weeks . each of these cats was subjected to a complete clinical examination and routine laboratory testing ( hematology , serum biochemistry , retroviral screening , and t4 concentration for cats > 7  years of age ) including fecal parasitologic examination and bacterial culture , and diagnostic imaging . a restriction diet trial was not administered in order to distinguish between these possibilities and thus the term samples of duodenal and colonic mucosa ( colonic mucosa was only collected from cats in the clinical group ) were collected by endoscopy as previously described.4 in brief , 6 biopsy specimens were fixed in 10% neutral buffered formalin , embedded in paraffin wax , sectioned at 5  m and stained with hematoxylin and eosin ( he ) . another set of 6 biopsy specimens was snapfrozen and stored at 80c until used for real time reverse transcriptasepolymerase chain reaction ( rtpcr ) . whenever possible , both inflamed and normal tissues were biopsied . biopsy specimens from all cats were scored for pathologic changes based on the architecture of the section and cellular infiltration of lamina propria in both villus and crypt areas . the study predated availability of the wsava gastrointestinal standardization group monograph11 but utilized a previously published scoring system.4 all slides were examined by a boardcertified veterinary pathologist ( mjd ) who was blinded to the animal 's identity . labeling for mhc class ii expression was performed using formalinfixed tissues and evaluated as previously described.4 , 5 briefly , for scoring epithelial expression of mhc class ii , areas in both crypt and villus epithelium were scored according to the intensity of mhc class ii labeling of the epithelial cells ( grades 04 ) . an overall score then was calculated by adding together the grades of all areas examined.5 for each group , the average and standard deviation of score in all cats then were calculated . the density of class ii cells in the lamina propria was scored from 1 to 4 using the following grading system : 
 normal density ( grade 1).mild increase in cellularity ( grade 2).increased cellularity ( grade 3).lamina propria densely populated with differentiated dendritic cells ( grade 4 ) . 
  normal density ( grade 1 ) . mild increase in cellularity ( grade 2 ) . increased cellularity ( grade 3 ) . all data were assessed for normal distribution using the normal probability plot before applying parametric or nonparametric analysis where appropriate . for detection of differences between groups , general linear model ( glm ) procedures were applied . when ftests were significant , student 's ttests were used to determine whether there were significant differences between the 2 groups for expression of mrna encoding cytokines and the presence of immune cells . pearson 's correlation coefficient test was used to check for positive or negative correlations between variables . all statistical analysis procedures were performed using statistical package for social scientists software.1 the significance level was set at p  <  .05 . isolation and dnase digestion of total rna from 2 to 4 endoscopic biopsy specimens ( 818  mg ) were performed as described previously.6 the quantity and quality of the resulting total rna were assessed by automated gel electrophoresis.2 il12p35 , il12p40 , ifn , and glyceraldehyde 3phosphate dehydrogenase ( g3pdh ) primers and probes were the kind gift of dr nghia van ngyun ( table  1).6 no felinespecific il12p19 sequence was available from genbank for the design of primers and probes for this target . therefore , a consensus sequence was obtained by aligning the human ( genbank accession number : nm_016584 ) , murine ( nm_031252 ) and canine ( xm_538231 ) sequences . consensus primers were designed using this consensus sequence ( forward : agagccagccagatytgagaag reverse : ctgctccrtgggcaaaga ) , which amplified a 580 base pair product from canine cdna . these primers were used to amplify products from feline intestine and lymph node cdna which were agarose gelpurified and sequenced.3 the sequence data generated from these experiments were submitted to genbank ( accession number : dq195102 ) . primers and probes were designed against the il23 p19 sequence using primer 3 ( www-genome.wi.mit.edu/cgi-bin/primer/primer3_www.cgi ) and mfold as described previously ( table  1).12 primers and probes were synthesized by eurogentec ltd4 and reconstituted in eb buffer ( 10  mm tris hcl ph8.45 ) before use . primer and probe sequences used in this study qrtpcr for il12 p35 , il12p40 , and ifn was carried out as previously described.6 
  the absence of genomic contamination of all rna samples was confirmed before the rt reactions by performing qpcr on the purified rna without reverse transcription with the g3pdh assay as previously described.6 none of the samples showed evidence of amplifiable genomic dna with this assay . a negative control of nucleasefree water and a positive control sample with a known ct value were included with all sample runs to control for runtorun ct variation . a pcr reaction was run for each rt repeat resulting in 2 ct values for each rna sample . g3pdh also was used as a  housekeeper gene to normalize all of the threshold cycle ( ct ) values of other cytokine products as previously described.6 
  in brief , a g3pdh ct value of 20 was chosen as a normalization value . the correction value for g3pdh of each sample the relative number of cdna copies in the sample was calculated using the following equation : relative cytokine copy number=2(42correctedcytokinectvalue ) 
  conventional pcr to obtain the amplicon for direct sequencing was carried out using the hotstartaq5 master mix as described previously6 but a thermocycling protocol of 95c for 15  minutes and 45 cycles of 95c for 15  seconds , 60c for 20  seconds , and 72c for 30  seconds before a final incubation at 72c for 5  minutes was used in a ptc200 dna engine.6 duodenal biopsy specimens were collected from control cats ( n  =  21 ) and cats with ibd or dietary hypersensitivity ( n  =  13 ) , collectively referred to as inflammatory enteropathy. control cats were specific pathogenfree ( spf ) animals 24  years of age with no history or clinical signs of gi disease . these animals were part of an experimental study , and the samples included in this study were taken before the start of the experiment . duodenal biopsy specimens were collected on 2 occasions from each cat and results represent an average of these 2 time points . the cats were kept under conditions approved by the uk home office and institutional ethical committee . cats with inflammatory enteropathy had evidence of vomiting , diarrhea , weight loss , or some combination of these signs for a minimum of 2  weeks . each of these cats was subjected to a complete clinical examination and routine laboratory testing ( hematology , serum biochemistry , retroviral screening , and t4 concentration for cats > 7  years of age ) including fecal parasitologic examination and bacterial culture , and diagnostic imaging . a restriction diet trial was not administered in order to distinguish between these possibilities and thus the term samples of duodenal and colonic mucosa ( colonic mucosa was only collected from cats in the clinical group ) were collected by endoscopy as previously described.4 in brief , 6 biopsy specimens were fixed in 10% neutral buffered formalin , embedded in paraffin wax , sectioned at 5  m and stained with hematoxylin and eosin ( he ) . another set of 6 biopsy specimens was snapfrozen and stored at 80c until used for real time reverse transcriptasepolymerase chain reaction ( rtpcr ) . biopsy specimens from all cats were scored for pathologic changes based on the architecture of the section and cellular infiltration of lamina propria in both villus and crypt areas . the study predated availability of the wsava gastrointestinal standardization group monograph11 but utilized a previously published scoring system.4 all slides were examined by a boardcertified veterinary pathologist ( mjd ) who was blinded to the animal 's identity . labeling for mhc class ii expression was performed using formalinfixed tissues and evaluated as previously described.4 , 5 briefly , for scoring epithelial expression of mhc class ii , areas in both crypt and villus epithelium were scored according to the intensity of mhc class ii labeling of the epithelial cells ( grades 04 ) . an overall score then was calculated by adding together the grades of all areas examined.5 for each group , the average and standard deviation of score in all cats then were calculated . the density of class ii cells in the lamina propria was scored from 1 to 4 using the following grading system : 
 normal density ( grade 1).mild increase in cellularity ( grade 2).increased cellularity ( grade 3).lamina propria densely populated with differentiated dendritic cells ( grade 4 ) . 
  normal density ( grade 1 ) . all data were assessed for normal distribution using the normal probability plot before applying parametric or nonparametric analysis where appropriate . for detection of differences between groups , general linear model ( glm ) procedures were applied . when ftests were significant , student 's ttests were used to determine whether there were significant differences between the 2 groups for expression of mrna encoding cytokines and the presence of immune cells . pearson 's correlation coefficient test was used to check for positive or negative correlations between variables . all statistical analysis procedures were performed using statistical package for social scientists software.1 the significance level was set at p  <  .05 . isolation and dnase digestion of total rna from 2 to 4 endoscopic biopsy specimens ( 818  mg ) were performed as described previously.6 the quantity and quality of the resulting total rna were assessed by automated gel electrophoresis.2 
  il12p35 , il12p40 , ifn , and glyceraldehyde 3phosphate dehydrogenase ( g3pdh ) primers and probes were the kind gift of dr nghia van ngyun ( table  1).6 no felinespecific il12p19 sequence was available from genbank for the design of primers and probes for this target . therefore , a consensus sequence was obtained by aligning the human ( genbank accession number : nm_016584 ) , murine ( nm_031252 ) and canine ( xm_538231 ) sequences . consensus primers were designed using this consensus sequence ( forward : agagccagccagatytgagaag reverse : ctgctccrtgggcaaaga ) , which amplified a 580 base pair product from canine cdna . these primers were used to amplify products from feline intestine and lymph node cdna which were agarose gelpurified and sequenced.3 the sequence data generated from these experiments were submitted to genbank ( accession number : dq195102 ) . primers and probes were designed against the il23 p19 sequence using primer 3 ( www-genome.wi.mit.edu/cgi-bin/primer/primer3_www.cgi ) and mfold as described previously ( table  1).12 primers and probes were synthesized by eurogentec ltd4 and reconstituted in eb buffer ( 10  mm tris  hcl ph8.45 ) before use . primer and probe sequences used in this study qrtpcr for il12 p35 , il12p40 , and ifn was carried out as previously described.6 
  the absence of genomic contamination of all rna samples was confirmed before the rt reactions by performing qpcr on the purified rna without reverse transcription with the g3pdh assay as previously described.6 none of the samples showed evidence of amplifiable genomic dna with this assay . a negative control of nucleasefree water and a positive control sample with a known ct value were included with all sample runs to control for runtorun ct variation . a pcr reaction was run for each rt repeat resulting in 2 ct values for each rna sample . g3pdh also was used as a  housekeeper gene to normalize all of the threshold cycle ( ct ) values of other cytokine products as previously described.6 
  in brief , a g3pdh ct value of 20 was chosen as a normalization value . the correction value for g3pdh of each sample . 
 corrected cytokine ct value = mean cytokine ctg3pdh correction value . 
  the relative number of cdna copies in the sample was calculated using the following equation : relative cytokine copy number=2(42correctedcytokinectvalue ) 
  conventional pcr to obtain the amplicon for direct sequencing was carried out using the hotstartaq5 master mix as described previously6 but a thermocycling protocol of 95c for 15  minutes and 45 cycles of 95c for 15  seconds , 60c for 20  seconds , and 72c for 30  seconds before a final incubation at 72c for 5  minutes was used in a ptc200 dna engine.6 isolation and dnase digestion of total rna from 2 to 4 endoscopic biopsy specimens ( 818  mg ) were performed as described previously.6 the quantity and quality of the resulting total rna were assessed by automated gel electrophoresis.2 il12p35 , il12p40 , ifn , and glyceraldehyde 3phosphate dehydrogenase ( g3pdh ) primers and probes were the kind gift of dr nghia van ngyun ( table  1).6 no felinespecific il12p19 sequence was available from genbank for the design of primers and probes for this target . therefore , a consensus sequence was obtained by aligning the human ( genbank accession number : nm_016584 ) , murine ( nm_031252 ) and canine ( xm_538231 ) sequences . consensus primers were designed using this consensus sequence ( forward : agagccagccagatytgagaag reverse : ctgctccrtgggcaaaga ) , which amplified a 580 base pair product from canine cdna . these primers were used to amplify products from feline intestine and lymph node cdna which were agarose gelpurified and sequenced.3 the sequence data generated from these experiments were submitted to genbank ( accession number : dq195102 ) . primers and probes were designed against the il23 p19 sequence using primer 3 ( www-genome.wi.mit.edu/cgi-bin/primer/primer3_www.cgi ) and mfold as described previously ( table  1).12 primers and probes were synthesized by eurogentec ltd4 and reconstituted in eb buffer ( 10  mm tris qrtpcr for il12 p35 , il12p40 , and ifn was carried out as previously described.6 
  the absence of genomic contamination of all rna samples was confirmed before the rt reactions by performing qpcr on the purified rna without reverse transcription with the g3pdh assay as previously described.6 none of the samples showed evidence of amplifiable genomic dna with this assay . a negative control of nucleasefree water and a positive control sample with a known ct value were included with all sample runs to control for runtorun ct variation . a pcr reaction was run for each rt repeat resulting in 2 ct values for each rna sample . g3pdh also was used as a  housekeeper gene to normalize all of the threshold cycle ( ct ) values of other cytokine products as previously described.6 
  in brief , a g3pdh ct value of 20 was chosen as a normalization value . the correction value for g3pdh of each sample was calculated as follows : g3pdh correction value = mean sample ct g3pdh value20 the relative number of cdna copies in the sample was calculated using the following equation : relative cytokine copy number=2(42correctedcytokinectvalue ) conventional pcr to obtain the amplicon for direct sequencing was carried out using the hotstartaq5 master mix as described previously6 but a thermocycling protocol of 95c for 15  minutes and 45 cycles of 95c for 15  seconds , 60c for 20  seconds , and 72c for 30  seconds before a final incubation at 72c for 5  minutes was used in a ptc200 dna engine.6 cats with inflammatory enteropathy were presented with chronic history of diarrhea ( n  =  13 ) , vomiting ( n  =  3 ) , weight loss ( n  =  13 ) , and all of these mentioned signs ( n  =  3 ) . the age of cats with inflammatory enteropathy ( n  =  13 ) ranged from 5 to 132  months ( mean , 51.43 ; median , 27 ) . breeds of cats in this group were domestic shorthair ( dsh ) , ragdoll , siamese , british blue , burmese , bengal , and norwegian forest . there was no sex predisposition and cats were male ( n  =  4 ) , female ( n  =  3 ) , neutered male ( n  =  4 ) , and neutered females ( n  =  2 ) . all the control group cats were dsh . both males ( n  =  13 ) and females ( n  =  8) were represented . details of age , sex , and breed distribution of both groups are summarized in table  2 . signalment of cats with inflammatory enteropathy and healthy controls mn , neutered male ; m , male ; fn , neutered female ; f , female ; min , minimum ; max , maximum age in the study group ; dsh , domestic shorthair . two groups were included in this study : cats with inflammatory enteropathy and healthy spf cats . histopathologic scores of healthy cats ranged from normal ( score  =  0 ) to moderate cellular infiltration ( score  =  2 ) ( mean , 0.8 , median , 1 ) . in cats with inflammatory enteropathy , duodenal biopsy specimens had an average score of 0.9 ( median , 1 ) , whereas colonic biopsy specimens had a consistent score of 2 ( moderate colitis ) even when no signs of colitis were reported by the owners ( mean , 1.63 , median , 2 ) . both the density of cells expressing mhc class ii within the duodenal lamina propria and the epithelial expression of this molecule by enterocytes were slightly higher in cats with inflammatory enteropathy than in healthy cats , but the difference was not significant ( p  >  .05 ) . mhc class ii 
  epithelial expression and lamina propria cell density scoring in duodenal biopsies of healthy controls and in cats with inflammatory enteropathy . il12p35 gene expression was significantly lower in duodenal biopsies of cats with inflammatory enteropathy than in healthy cats ( p  =  .0001 ) , whereas p40 gene expression was not significantly different between the 2 groups ( p  =  .079 ) . il23p19 mrna was significantly higher in duodenal biopsies of cats with inflammatory enteropathy than in healthy cats ( p  =  .001 ) , but ifn gene expression was not significantly different between the 2 groups ( p  =  .993 ) . il12 p35 , p40 , and ifng mrna expression in duodenal biopsies of control cats and cats with inflammatory enteropathy . il23p19 mrna expression levels in duodenal biopsies of healthy cats and cats with inflammatory enteropathy . there was a positive correlation between all measured cytokines for the control group ( p  <  .001 ; table  3 ) . there was a highly significant positive correlation between il12p40 and il12p35 gene expression ( p  =  .001 ) in duodenal biopsies of cats with inflammatory enteropathy ( table  4 ) . il23p19 gene expression was positively correlated with that for il12p35 ( p  =  .04 ) , il12p40 ( p  =  .002 ) , and ifn ( p  =  .015 ) in the duodenal biopsies of cats with inflammatory enteropathy . ifn mrna was not significantly correlated with that encoding il12p40 ( p  >  .05 ) . cytokine mrna correlation in duodenal biopsies of control cats the values presented are the pearson correlation coefficient . cytokine mrna correlations in duodenal biopsies of cats with inflammatory enteropathy the values presented are the pearson correlation coefficient . cats with inflammatory enteropathy were presented with chronic history of diarrhea ( n  =  13 ) , vomiting ( n  =  3 ) , weight loss ( n  =  13 ) , and all of these mentioned signs ( n  =  3 ) . the age of cats with inflammatory enteropathy ( n  =  13 ) ranged from 5 to 132  months ( mean , 51.43 ; median , 27 ) . breeds of cats in this group were domestic shorthair ( dsh ) , ragdoll , siamese , british blue , burmese , bengal , and norwegian forest . there was no sex predisposition and cats were male ( n  =  4 ) , female ( n  =  3 ) , neutered male ( n  =  4 ) , and neutered females ( n  =  2 ) . all the control group cats were dsh . both males ( n  =  13 ) and females ( n  =  8) were represented . details of age , sex , and breed distribution of both groups are summarized in table  2 . signalment of cats with inflammatory enteropathy and healthy controls mn , neutered male ; m , male ; fn , neutered female ; f , female ; min , minimum ; max , maximum age in the study group ; dsh , domestic shorthair . two groups were included in this study : cats with inflammatory enteropathy and healthy spf cats . histopathologic scores of healthy cats ranged from normal ( score  =  0 ) to moderate cellular infiltration ( score  =  2 ) ( mean , 0.8 , median , 1 ) . in cats with inflammatory enteropathy , duodenal biopsy specimens had an average score of 0.9 ( median , 1 ) , whereas colonic biopsy specimens had a consistent score of 2 ( moderate colitis ) even when no signs of colitis were reported by the owners ( mean , 1.63 , median , 2 ) . both the density of cells expressing mhc class ii within the duodenal lamina propria and the epithelial expression of this molecule by enterocytes were slightly higher in cats with inflammatory enteropathy than in healthy cats , but the difference was not significant ( p  >  .05 ) . mhc class ii 
  epithelial expression and lamina propria cell density scoring in duodenal biopsies of healthy controls and in cats with inflammatory enteropathy . il12p35 gene expression was significantly lower in duodenal biopsies of cats with inflammatory enteropathy than in healthy cats ( p  =  .0001 ) , whereas p40 gene expression was not significantly different between the 2 groups ( p  =  .079 ) . il23p19 mrna was significantly higher in duodenal biopsies of cats with inflammatory enteropathy than in healthy cats ( p  =  .001 ) , but ifn gene expression was not significantly different between the 2 groups ( p  =  .993 ) . il12 p35 , p40 , and ifng mrna expression in duodenal biopsies of control cats and cats with inflammatory enteropathy . il23p19 mrna expression levels in duodenal biopsies of healthy cats and cats with inflammatory enteropathy . there was a positive correlation between all measured cytokines for the control group ( p  <  .001 ; table  3 ) . there was a highly significant positive correlation between il12p40 and il12p35 gene expression ( p  =  .001 ) in duodenal biopsies of cats with inflammatory enteropathy ( table  4 ) . il23p19 gene expression was positively correlated with that for il12p35 ( p  =  .04 ) , il12p40 ( p  =  .002 ) , and ifn ( p  =  .015 ) in the duodenal biopsies of cats with inflammatory enteropathy . ifn mrna was not significantly correlated with that encoding il12p40 ( p  >  .05 ) . cytokine mrna correlation in duodenal biopsies of control cats the values presented are the pearson correlation coefficient . cytokine mrna correlations in duodenal biopsies of cats with inflammatory enteropathy the values presented are the pearson correlation coefficient . this study characterized il23 p19 gene expression in the duodenal mucosa of healthy cats and cats with chronic idiopathic inflammatory enteropathy . such analysis has not been performed previously in cats or dogs with ibd . as reported in the literature , cats referred with chronic signs of inflammatory enteropathy were middle to olderaged animals.13 there was no breed predilection , although there were relatively more dsh and ragdoll cats ( n  =  5 and 2 , respectively ) , but the study sample was relatively small . significant differences in the levels of expression of mrna encoding il12p40 , but not il12p35 have been reported between the healthy cats and the cats with histologic evidence of intestinal inflammation.6 since that study , another cytokine has been characterized which shares the p40 subunit with il12 and is now referred to as il23.9 in light of these new findings , the observed increase in expression of the il12 p40 gene reported in cats could indicate translation into il23 , rather than il12 , protein . all cats included in the clinical group of this study had histopathologic changes suggestive of ibd , but some cats in the control group also had mild inflammatory infiltration of the duodenal mucosa . we have noted the presence of such inflammation in clinically normal cats of this experimentally housed colony in previous investigations.6 evaluation of cellular infiltration in hestained endoscopic biopsy specimens can be difficult , but evaluation has now been simplified by availability of the standards published by the world small animal veterinary association ( wsava ) gastrointestinal standardization group.11 in this study , there was no interobserver variation because all biopsies were evaluated on 1 occasion by a single pathologist . spfderived cats may differ from healthy pet cats , but ethical and legal constraints prevented sampling the intestinal mucosa of clinically normal pet animals . dilemmas in the choice of a control group also apply to clinical studies of gi disease in humans and dogs where similar ethical constraints related to the availability of patient tissue arise . mhc class ii expression by epithelial cells was higher in cats with inflammatory enteropathy , although the increased level of expression was not significant . we have previously shown that mhc class ii expression was significantly upregulated in cats with ibd as compared to cats with gi disease or healthy controls.4 in this study , the number of cases included was smaller than in the previous study . this may explain the lack of significant difference despite the higher expression score obtained for the cats with inflammatory enteropathy . il12p40 and ifn gene expression was not significantly different between the 2 groups , whereas il12p35 mrna was significantly lower in cats with inflammatory enteropathy . il12p40 mrna was highly significantly correlated with p19 mrna in cats with inflammatory enteropathy . unlike in the previous report6 , il12p35 mrna was significantly lower in cats with inflammatory enteropathy . significant variation in the level of expression of mrna encoding il23p19 after the introduction of novel diets to clinically healthy cats has been observed ( n.e . , these results support the hypothesis that il23 is implicated in the immunopathogenesis of feline inflammatory enteropathy . the significant positive correlation between ifn , il23p19 , and il12p35 suggest that all of these cytokines may still have a role in the pathogenesis of gi inflammation in cats . the 2 major forms of ibd in humans are crohn 's disease ( cd ) and ulcerative colitis ( uc ) . cd has been associated with a th1dominated cytokine profile , whereas a th2 cytokine response has been linked to uc.14 il23 is now known to play an important role in the pathogenesis of cd in humans.14 , 15 an il12driven th1 response may dominate during the early stages of cd , implying that susceptibility to il12mediated modulation is strongly dependent on the stage of the disease,16 although activities that have been attributed to il12 in the past may have been mediated by il23.17 several studies have now demonstrated an important role for th17 cells in intestinal inflammation.18 , 19 
  gi inflammation in cats also has a complicated immunopathogenesis which involves both proinflammatory and immunoregulatory cytokines.6 , 7 the results of this study add to this complexity by showing for the first time that there is significant upregulation of il23 gene expression in the duodenal mucosa of cats with inflammatory enteropathy . this suggests that in feline chronic inflammatory enteropathy , a th17type response also may occur .
backgrounddietary hypersensitivity and inflammatory bowel disease ( ibd ) are important causes of chronic vomiting and diarrhea in cats . 
 il23 has been recently found to be a key factor in the immunopathogenesis of ibd in humans but the involvement in ibd has not been investigated in cats.hypothesis/objectivesexpression of genes encoding il12p35 and p40 , il23p19 , and ifn may be upregulated in duodenal biopsy specimens taken from cats with histologic evidence of inflammation.animals and methodsduodenal biopsy specimens were collected from control cats ( n  =  21 ) and cats with inflammatory enteropathy ( n  =  13 ) . 
 routine histopathology , immunohistochemistry ( ihc ) , and qrtpcr were used to assess expression of mhc class ii and to measure gene transcripts encoding the p35 , p40 , and p19 subunits of the il12 family of cytokines and ifn.resultsthere were significant differences in expression of mrna encoding il12p35 and il23p19 between healthy cats and cats with inflammatory enteropathy . 
 il12p35 mrna was lower in the duodenal mucosa of cats with inflammatory enteropathy compared with the mucosa of healthy cats ( p  =  .001 ) . 
 in contrast , il23p19 mrna expression was higher in duodenal biopsy specimens from cats with inflammatory enteropathy than in those from healthy controls ( p  =  .001 ) . 
 there was no difference in expression of il12p40 and ifn mrna ( p  >  .05 ) . 
 the majority of cats with inflammatory enteropathy had histologic evidence of moderate to severe colitis ( score 2).conclusions and clinical importancethe results of this preliminary study suggest that il23 plays a role in the pathogenesis of feline inflammatory enteropathy .