Increased interleukin-2 messenger RNA in the intestinal mucosal lesions of Crohn's disease but not ulcerative colitis

Mullin, Gerard E.; Lazenby, Audrey J.; Harris, Mary L.; Bayless, Theodore M.; James, Stephen P.

doi:10.1016/0016-5085(92)91722-g

Cited by 195 publications

(91 citation statements)

References 36 publications

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“…The presence of large numbers of activated T cells in the involved mucosa of IBD patients suggests that IL2 is likely to be playing at least some role in stimulating inflammation [61,62]. This study revealed no association of the IL2 polymorphism with IBD in our patient population.…”

Section: Discussioncontrasting

confidence: 47%

Replication of Identified Inflammatory Bowel Diseases Genetic Associations: A Case–Control Study in the Tunisian Population

Bouzid¹

2013

J Clin Cell Immunol

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Inflammatory bowel diseases (IBD) -Crohn's disease (CD) and ulcerative colitis (UC) -are chronic gastrointestinal inflammatory disorders with a complex genetic background. A genome wide association scan by the Welcome Trust Case Control Consortium (WTCCC) recently identified several novel susceptibility loci. We performed a replication study in 107 IBD patients (39 CD and 68 UC) and 162 controls. In total, 19 single nucleotide polymorphisms (SNPs) from previously identified susceptibility genes PTPN11, TNF α, IL23R, PTPN2, PTPN22, IL2 and IL10 were studied. In UC, we confirmed the association with PTPN2 (rs254215, GG, P=0.013, P corr =0.039; OR= 6.23 (1.18; 32.95)). In CD, we confirmed a marginal association with ((rs11066320, GG, P=0.018, P corr =0.054, OR= 0.4 (0.19; 0.82)). No significant association was found at the allele and genotype levels of SNPs in TNF α, IL23R, PTPN22, IL2, and IL10. However, on the haplotype analysis the AG haplotype of TNFα was more frequent in CD patients compared to controls (23.1% vs. 13.7%; P = 0.039; OR= 1.89 (1.02; 3.5)). The PTPN11 ATG haplotype was also more frequent in CD patients compared to controls (32.1% vs 21.3%; P = 0.04; OR= 1.75 (1.01; 3.01). These results reveal limited replication in Tunisian population and indicate differences in genetic architecture between populations.

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Section: Discussioncontrasting

confidence: 47%

Replication of Identified Inflammatory Bowel Diseases Genetic Associations: A Case–Control Study in the Tunisian Population

Bouzid¹

2013

J Clin Cell Immunol

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“…Some IBD patients have a decreased mucosal IL-4 production [26] and in some experimental colitis models, such as in IL-2 knockout mice [27], IL-4 production is down-regulated. In contrast to CD, UC has no such typical Th1 cytokine pattern [23,28]. In DSS-induced colitis, a UC-like model, IL-4 secretion is up-regulated during its chronic phase.…”

Section: Discussionmentioning

confidence: 99%

Chronic experimental colitis induced by dextran sulphate sodium (DSS) is characterized by Th1 and Th2 cytokines

Dieleman¹,

Palmen²,

Akol³

et al. 1998

Clinical and Experimental Immunology

974

735

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SUMMARYOral administration of DSS has been reported to induce an acute and chronic colitis in mice. The aim of our study was to evaluate if the chronic phase of DSS-induced colitis was characterized by a Th1/Th2 response and how this would relate to mucosal regeneration. Swiss Webster mice were fed 5% DSS in their drinking water for 7 days, followed by 2-5 weeks consumption of water. Control mice received only water. The animals were killed at 3 and 6 weeks after induction. Their colons were isolated for histology and immunohistochemistry, using specific MoAbs for T and B cells, macrophages, interferon-gamma (IFNg), IL-4 and IL-5. Colons were scored for inflammation, damage and regeneration. Two weeks after stopping DSS the colonic epithelium had only partially healed. Total colitis scores were still increased, especially in the distal colon, which was due to more inflammation, damage and less regeneration. In areas of incomplete colonic healing the basal parts of the lamina propria contained macrophages and CD4 þ T cells. These CD4 þ T cells showed a focal increase of IFN-g and IL-4 staining compared with control animals. These findings were still observed 5 weeks after stopping DSS in some mice, albeit less extensive. Chronic DSS-induced colitis is characterized by focal epithelial regeneration and a Th1 as well as Th2 cytokine profile. We postulate that chronic immune activation mediated by both populations of Th cells can interfere with colonic healing and can play a role in the pathogenesis of chronic colitis.

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“…As only small amounts of total cellular RNA could be extracted from the liver biopsies available for the present study, a RT-PCR method for determining individual cytokine mRNAs was applied. This method has the advantage of being both sensitive, and, when appropriate controls are used, quantitative [24][25][26].…”

Section: Discussionmentioning

confidence: 99%

Cytokine mRNA expression in the liver of patients with primary biliary cirrhosis (PBC) and chronic hepatitis B (CHB)

Shindo¹,

Mullin

Braun-Elwert

et al. 1996

Clinical and Experimental Immunology

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SUMMARYThe expression of cytokine mRNA species was determined in liver biopsies from six normal subjects, 18 patients with PBC and 14 patients with hepatitis B e antigen (HBeAg)-positive CHB using a reverse transcriptase-polymerase chain reaction (RT-PCR) technique. cDNA, obtained by reverse transcription using oligo d(T) primers, was amplified by PCR using primers specific for the coding region of seven different cytokines (IL-1, IL-2, IL-4, IL-5, IL-6, interferon-gamma (IFN-°), tumour necrosis factoralpha (TNF-®)). The abundance of some cytokines (IL-2, IL-4, IL-5 and IFN-°) was also estimated by semiquantitative RT-PCR, using as standards dilutions of synthetic cytokine mRNA transcripts, that could be distinguished electrophoretically from respective native cytokine mRNAs. Hepatic inflammation was assessed by a semiquantitative histologic score and by amplification of mRNA for T cell receptor (TCR)-®. mRNAs for IL-1 and IL-6 were detected in only one control liver. In CHB, mRNAs for IL-1, IL-2, IL-4, IL-5 and IFN-°were detected in 43%, 60%, 80%, 20%, and 54% of biopsies, respectively. mRNA for IFN-°and IL-4, but not IL-1, tended to be associated with severe inflammation. In five biopsies semiquantitative analyses revealed increased levels of mRNA for TCR-® and, when transcripts were detectable, high levels of mRNA for IFN-°and IL-4. In PBC, mRNA for IFN-°was detected in 60% of biopsies, but no mRNAs for IL-1, IL-2, IL-4, IL-5, or IL-6, or for TNF-®, were detected. Semiquantitative analyses revealed that absolute levels of mRNA for IFN-°tended to correlate with the severity of hepatic inflammation. The results suggest that: (i) there may be fundamental differences in the roles that cytokines play in the hepatic inflammatory processes of PBC and CHB; and (ii) while hepatic IFN-°mRNA expression is not specific for PBC, IFN-°may play a prominent role in the immunopathogenesis of PBC.

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Increased interleukin-2 messenger RNA in the intestinal mucosal lesions of Crohn's disease but not ulcerative colitis

Cited by 195 publications

References 36 publications

Replication of Identified Inflammatory Bowel Diseases Genetic Associations: A Case–Control Study in the Tunisian Population

Replication of Identified Inflammatory Bowel Diseases Genetic Associations: A Case–Control Study in the Tunisian Population

Chronic experimental colitis induced by dextran sulphate sodium (DSS) is characterized by Th1 and Th2 cytokines

Cytokine mRNA expression in the liver of patients with primary biliary cirrhosis (PBC) and chronic hepatitis B (CHB)

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