Lack of autoantibodies against collagen and related proteins in collagenous colitis
(2022) In BMC Immunology 23(1). p.29-29- Abstract
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... (More)
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.
(Less)
- author
- Larsson, Jk LU ; Roth, B LU ; Ohlsson, B LU and Sjöberg, K LU
- organization
- publishing date
- 2022-06-06
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Autoantibodies, Autoimmunity, Collagen type III, Collagen type IV, Collagenous colitis, MMP-9, Tenascin, TIMP-1
- in
- BMC Immunology
- volume
- 23
- issue
- 1
- pages
- 1 pages
- publisher
- BioMed Central (BMC)
- external identifiers
-
- scopus:85131342914
- pmid:35668375
- ISSN
- 1471-2172
- DOI
- 10.1186/s12865-022-00504-5
- language
- English
- LU publication?
- yes
- id
- 6c9174d3-12c3-49ea-bd5d-5f7a0e1a7b16
- date added to LUP
- 2022-10-14 15:45:21
- date last changed
- 2024-11-01 12:19:51
@article{6c9174d3-12c3-49ea-bd5d-5f7a0e1a7b16, abstract = {{<p>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. </p>}}, author = {{Larsson, Jk and Roth, B and Ohlsson, B and Sjöberg, K}}, issn = {{1471-2172}}, keywords = {{Autoantibodies; Autoimmunity; Collagen type III; Collagen type IV; Collagenous colitis; MMP-9; Tenascin; TIMP-1}}, language = {{eng}}, month = {{06}}, number = {{1}}, pages = {{29--29}}, publisher = {{BioMed Central (BMC)}}, series = {{BMC Immunology}}, title = {{Lack of autoantibodies against collagen and related proteins in collagenous colitis}}, url = {{http://dx.doi.org/10.1186/s12865-022-00504-5}}, doi = {{10.1186/s12865-022-00504-5}}, volume = {{23}}, year = {{2022}}, }