ArticleDigestive diseases and sciences2003
Immunolocalization and expression of kallistatin and tissue kallikrein in human inflammatory bowel disease.
Article in Digestive diseases and sciences, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 31 citations in OpenAlex.
- The Serine Protease-Serine Protease Inhibitor Regulatory Network in Inflammatory Bowel Disease: From Molecular Mechanisms to Novel Therapeutic Horizons.Journal of advanced research · 2026Review
- Proteases in intestinal health and disease.Nature reviews. Gastroenterology & hepatology · 2026Review
- Cardiovascular manifestations of inflammatory bowel diseases and the underlying pathogenic mechanisms.American journal of physiology. Regulatory, integrative and comparative physiology · 2023Review
- Protective Role of Endogenous Kallistatin in Vascular Injury and Senescence by Inhibiting Oxidative Stress and Inflammation.Oxidative medicine and cellular longevity · 2018Review
- Human kallistatin administration reduces organ injury and improves survival in a mouse model of polymicrobial sepsis.Immunology · 2014Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
The distribution of tissue kallikrein (TK) and its plasma inhibitor, kallistatin in plasma and intestinal tissue, was studied in patients with active ulcerative colitis (UC) and Crohn's disease (CD). TK was localized to goblet cells and kallistatin to epithelial cells of normal human intestine. Both proteins are visualized in macrophages inside granulomas in CD as well as in plasmocytes in both CD and UC. Intestinal tissue kallikrein (ITK) and kallistatin are significantly decreased in inflamed intestine compared to noninflammatory controls. TK mRNA is significantly decreased in intestinal biopsy samples from active UC patients compared with inactive patients or controls. Immunoreactive TK is present in plasma in very low concentrations in patients and did not differ in normal subjects. Plasma kallistatin was significantly decreased in patients with active disease compared to normal controls. Our data suggest that release of TK during inflammation plays a role in inflammatory bowel disease.
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Registered trials
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