P069. High autofluorescence of the colon tissues in children with ulcerative colitis
E. Jarocka-Cyrta1, J. Branska-Januszewska2, M. Kaczmarski3, H. Ostrowska2, 1University of Warmia and Masuria, Department of Pediatrics, Olsztyn, Poland, 2Medical University of Bialystok, Department of Biology, Bialystok, Poland, 3Medical University of Bialystok, Department of Pediatrics, Gastroenterology and Allergology, Bialystok, Poland
Inflammatory bowel disease (IBD) is characterized by chronic inflammation of the gastrointestinal tract. There is a growing body of evidence suggesingt that sustained gut inflammation is associated with enhanced oxidative stress. Oxidative stress is one of the factors responsible for protein misfolding and damage. Oxidatively modified proteins can aggregate into small inclusion bodies termed the aggresome or aggresome-like induced structures (ALIs), and if not degraded, they can be precursors of autofluorescent highly oxidized cross-linked aggregates, known as lipofuscin or advanced glycooxidation end products (AGEs). The formation of these inclusion bodies is tightly associated with inflammatory responses and cell death.
The aim of the study was to analyse the presence of inclusion bodies in colonic tissue of children with ulcerative colitis (CU).
Biopsy samples were taken from the colon during colonoscopy/sigmoidoscopy from 30 UC children (16 girls; median age 15.0 years; range 4.33–17.83) and 10 controls (5 girls; median age 13.0 years; range 2.42–17.83).
Inclusion bodies were identified on paraffine-embedded colon biopsies on the basis of autofluorescence using fluorescence microscope with confocal imaging system - Nikon ECLIPSE Ti/C1 Plus (Ex 543 nm/Em 605 nm). Aggresome structures were detected using a commercially available ProteoStat® Aggresome Detection Kit (Enzo Life Science, Inc.).
The quantity of autofluorescent inclusion bodies was significantly higher in patients with CU than in the control group. These round or dotty perinuclear structures were present exclusively in mononuclear inflammatory cells in lamina propria both in patients in the active stage of CU and those in remission. The autofluorescent protein aggregates were also detected extracellularly. These autofluorescent structures colocalized with the signal obtained with the commercially available aggresome detection kit.
Our study demonstrates for the first time, that colon tissue in children with ulcerative colitis contains a high amount of autofluorescent inclusion bodies in mononuclear inflammatory cells, and of extracellular autofluorescent protein aggregates, regardless of disease stage. We propose that these structures might represent aggresomes and related inclusion bodies and could act as a triggering factor of sustained inflammatory processes in CU.