Abstract
Intestinal fatty acid binding protein (I-FABP) indicates barrier integrity. Aims: determine if I-FABP is elevated in active Crohn's disease (CD) and if I-FABP parallels anti-TNFα antibody (infliximab) induced lowering of TNFα and Harvey-Bradshaw Index (HBI) as potential indicator of mucosal healing. I-FABP distribution along human gut was determined. Serum from 10 CD patients collected during first three consecutive infliximab treatments with matched pretreatment and follow-up samples one week after each treatment and corresponding HBI data were analyzed. I-FABP reference interval was established from 31 healthy subjects with normal gut permeability. I-FABP and TNFα were measured by ELISA; CRP was measured by nephelometry. Healthy tissue was used for I-FABP immunohistochemistry. Pretreatment CD patient TNFα was 1.6-fold higher than in-house reference interval, while I-FABP was 2.5-fold higher, which lowered at follow-ups. Combining all 30 infusion/follow-up pairs also revealed changes in I-FABP. HBI followed this pattern; CRP declined gradually. I-FABP was expressed in epithelium of stomach, jejunum, ileum, and colon, with the highest expression in jejunum and ileum. I-FABP is elevated in active CD with a magnitude comparable to TNFα. Parallel infliximab effects on TNFα, HBI, and I-FABP were found. I-FABP may be useful as an intestine selective prognostic marker in CD.
Highlights
The gastrointestinal (GI) tract maintains a barrier against harmful agents by means of the epithelial mucosa, which is compromised in many disorders and/or diseases
Intestinal fatty acid binding protein (I-FABP) Is Elevated in Active Crohn’s disease (CD) and Parallels TNFα and Harvey-Bradshaw Index (HBI)
Our main purpose was to determine if treatment outcomes could be monitored with I-FABP in the context of mucosal healing estimation in active CD patients
Summary
The gastrointestinal (GI) tract maintains a barrier against harmful agents (e.g., xenobiotics) by means of the epithelial mucosa, which is compromised in many disorders and/or diseases. This defense barrier is comprised of a single layer of columnar epithelial cells lining the lumen. It possesses a regulated permeability function by way of tight junctions as well as a mucopolysaccharide covering. Factors (e.g., environmental and dietary, particulate matter, high-fat diet) that damage enterocytes compromise intestinal immune defenses [3, 4] According to Montreal phenotype classification, unlike ulcerative colitis (UC), the inflammatory site in CD can occur at any part of the GI tract, characterized by segmental transmural inflammation, with more pronounced necrosis of the affected epithelium having the potential of manifesting extraintestinal immunopathy-associated symptoms [6]
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