PMID- 35668375 OWN - NLM STAT- MEDLINE DCOM- 20220608 LR - 20220716 IS - 1471-2172 (Electronic) IS - 1471-2172 (Linking) VI - 23 IP - 1 DP - 2022 Jun 6 TI - Lack of autoantibodies against collagen and related proteins in collagenous colitis. PG - 29 LID - 10.1186/s12865-022-00504-5 [doi] LID - 29 AB - INTRODUCTION: Collagenous colitis (CC) is a common cause of chronic diarrhea and is characterized by a subepithelial thickened collagen layer in the colonic mucosa. It shares many of the characteristics found in autoimmune diseases, but no autoantibodies have been identified. In CC, an imbalance in collagen turnover is evident. The purpose of the present study was to investigate whether any collagen-associated autoantibodies or other antibodies such as TPO and ASCA were present, and if levels of total IgE were increased. METHODS: Sera from women with active CC were analysed with ELISA for detection of autoantibodies against collagen type III and IV (Col III and IV), matrix metalloproteinase-9 (MMP-9), tissue inhibitors of metalloproteinase-1 (TIMP-1) and tenascin-C (TNC). Sera were also analysed for TPO, ASCA and total IgE. Healthy female blood donors served as controls. The cut-off value in the control group was defined as relative units > 97.5th percentile. RESULTS: Sixty-six women were included (mean age 60 years; range 31-74, mean disease duration 6 years; range 1-22). No autoantibody was significantly overexpressed in the CC population compared to controls. The mean disease duration was lower (p = 0.03) in the subjects who expressed collagen-associated autoantibodies (3.7 years; range 1-14), compared to those who did not (6.4 years; range 1-22). Treatment with budesonide was not associated with any of these autoantibodies. CONCLUSION: No increased presence of the investigated antibodies could be found in the present study of CC. Neither could antibodies against ASCA or TPO, or elevated levels of IgE, be found. Consequently, no association was found between CC and these proteins, even though this may not be generalizable to other compounds in the collagen layer. CI - (c) 2022. The Author(s). FAU - Jk, Larsson AU - Jk L AD - Department of Clinical Sciences, Department of Gastroenterology and Nutrition, Lund University, Skane University Hospital, Malmo, Sweden. johanna.larsson@med.lu.se. FAU - B, Roth AU - B R AD - Department of Clinical Sciences, Department of Gastroenterology and Nutrition, Lund University, Skane University Hospital, Malmo, Sweden. FAU - B, Ohlsson AU - B O AD - Department of Clinical Sciences, Department of Medicine, Lund University, Skane University Hospital, Malmo, Sweden. FAU - K, Sjoberg AU - K S AD - Department of Clinical Sciences, Department of Gastroenterology and Nutrition, Lund University, Skane University Hospital, Malmo, Sweden. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20220606 PL - England TA - BMC Immunol JT - BMC immunology JID - 100966980 RN - 0 (Autoantibodies) RN - 37341-29-0 (Immunoglobulin E) RN - 9007-34-5 (Collagen) SB - IM MH - Adult MH - Aged MH - Autoantibodies MH - *Colitis/complications/metabolism MH - *Colitis, Collagenous/complications MH - Collagen/metabolism MH - Female MH - Humans MH - Immunoglobulin E MH - Middle Aged PMC - PMC9171945 OTO - NOTNLM OT - Autoantibodies OT - Autoimmunity OT - Collagen type III OT - Collagen type IV OT - Collagenous colitis OT - MMP-9 OT - TIMP-1 OT - Tenascin COIS- The authors declare that they have no competing interests. EDAT- 2022/06/07 06:00 MHDA- 2022/06/09 06:00 PMCR- 2022/06/06 CRDT- 2022/06/06 23:29 PHST- 2021/12/14 00:00 [received] PHST- 2022/06/01 00:00 [accepted] PHST- 2022/06/06 23:29 [entrez] PHST- 2022/06/07 06:00 [pubmed] PHST- 2022/06/09 06:00 [medline] PHST- 2022/06/06 00:00 [pmc-release] AID - 10.1186/s12865-022-00504-5 [pii] AID - 504 [pii] AID - 10.1186/s12865-022-00504-5 [doi] PST - epublish SO - BMC Immunol. 2022 Jun 6;23(1):29. doi: 10.1186/s12865-022-00504-5.