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2 results on '"early interleukin-33 expression"'

1. Interleukin-33 exacerbates acute colitis via interleukin-4 in mice.

Author

Pushparaj, Peter N., Li, Dong, Komai‐Koma, Mousa, Guabiraba, Rodrigo, Alexander, James, McSharry, Charles, and Xu, Damo

Subjects
*INTERLEUKIN-33, *COLITIS, *INTERLEUKIN-4, *LABORATORY mice, *INTERLEUKIN receptors, *SCIENTIFIC observation, *GENE expression
Abstract

Interleukin-33 ( IL-33) and its receptor ST2 are over-expressed in clinical colitis tissue. However, the significance of these observations is at present unknown. Significantly, we demonstrate here that IL33 and ST2 are the primary early genes induced in the inflamed colon of BALB/c mice following dextran sulphate sodium ( DSS)-induced experimental ulcerative colitis. Accordingly diarrhoea and DSS-induced colon inflammation were impaired in ST2−/− BALB/c mice and exacerbated in wild-type mice by treatment with exogenous recombinant IL-33, associated respectively with reduced and enhanced expression of chemokines ( CXCL9 and CXCL10), and inflammatory ( IL-4, IL-13, IL-1, IL-6, IL-17) and angiogenic (vascular endothelial growth factor) cytokines in vivo. The exacerbation effect of treatment with recombinant IL-33 on DSS-induced acute colitis was abolished in IL-4−/− BALB/c mice. Hence, IL-33 signalling via ST2, by inducing an IL-4-dependent immune response, may be a major pathogenic factor in the exacerbation of ulcerative colitis. [ABSTRACT FROM AUTHOR]

Published
2013
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2. Interleukin-33 exacerbates acute colitis via interleukin-4 in mice

Author

James Alexander, Peter Natesan Pushparaj, Damo Xu, Rodrigo Guabiraba, Mousa Komai-Koma, Dong Li, Charles McSharry, Institute of Infection, Immunity and Inflammation, University of Glasgow, King Abdulaziz University, Umm Al-Qura University, Infectiologie et Santé Publique (UMR ISP), Institut National de la Recherche Agronomique (INRA)-Université de Tours, Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde [Glasgow], Arthritis Research UK, Medical Research Council UK, Wellcome Trust, UK, and Institut National de la Recherche Agronomique (INRA)-Université de Tours (UT)

Subjects
Chemokine, Exacerbation, colitis, Immunology, Gene Expression, 03 medical and health sciences, Mice, 0302 clinical medicine, Immunology and Allergy, Medicine, Animals, Colitis, interleukin-4 deficiency, Interleukin 4, Acute colitis, 030304 developmental biology, ST2 deficiency, Mice, Knockout, 0303 health sciences, Mice, Inbred BALB C, biology, business.industry, Interleukins, Receptors, Interleukin, Original Articles, medicine.disease, Interleukin-33, Ulcerative colitis, Interleukin-1 Receptor-Like 1 Protein, early interleukin-33 expression, 3. Good health, Receptors, Interleukin-4, Interleukin 33, 030220 oncology & carcinogenesis, Acute Disease, biology.protein, CXCL9, [SDV.IMM]Life Sciences [q-bio]/Immunology, Cytokines, Colitis, Ulcerative, Female, Interleukin-4, Chemokines, Inflammation Mediators, business, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology, Signal Transduction
Abstract

Pushparaj, Peter N Li, Dong Komai-Koma, Mousa Guabiraba, Rodrigo Alexander, James McSharry, Charles Xu, Damo Arthritis Research UK/United Kingdom Medical Research Council/United Kingdom Wellcome Trust/United Kingdom England Immunology. 2013 Sep;140(1):70-7. doi: 10.1111/imm.12111.; International audience; Interleukin-33 (IL-33) and its receptor ST2 are over-expressed in clinical colitis tissue. However, the significance of these observations is at present unknown. Significantly, we demonstrate here that IL33 and ST2 are the primary early genes induced in the inflamed colon of BALB/c mice following dextran sulphate sodium (DSS)-induced experimental ulcerative colitis. Accordingly diarrhoea and DSS-induced colon inflammation were impaired in ST2(-/-) BALB/c mice and exacerbated in wild-type mice by treatment with exogenous recombinant IL-33, associated respectively with reduced and enhanced expression of chemokines (CXCL9 and CXCL10), and inflammatory (IL-4, IL-13, IL-1, IL-6, IL-17) and angiogenic (vascular endothelial growth factor) cytokines in vivo. The exacerbation effect of treatment with recombinant IL-33 on DSS-induced acute colitis was abolished in IL-4(-/-) BALB/c mice. Hence, IL-33 signalling via ST2, by inducing an IL-4-dependent immune response, may be a major pathogenic factor in the exacerbation of ulcerative colitis.

Published
2013

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