Open AccessHumoral response to Clostridium difficile in inflammatory bowel disease, including correlation with immunomodulatory treatment
Author(s) -
Henriksson Gunnel,
Bredberg Johan,
Wullt Marlene,
Lyrenäs Ebbe,
Hindorf Ulf,
Ohlsson Björn,
Grip Olof
Publication year - 2019
Publication title -
jgh open
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.546
H-Index - 8
ISSN - 2397-9070
DOI - 10.1002/jgh3.12122
Subject(s) - clostridium difficile , clostridium difficile toxin a , inflammatory bowel disease , immune system , ulcerative colitis , immunology , pathogenesis , clostridium difficile toxin b , toxin , disease , humoral immunity , medicine , colitis , immunoglobulin a , microbiology and biotechnology , immunoglobulin g , biology , antibiotics
Background and Aim An abnormal immune response to intestinal bacteria has been observed in Crohn's disease (CD). Clostridium difficile infection incidence and severity are increased in CD, but reports on the humoral response have provided conflicting results. We aimed to shed light on the possible role of C. difficile in CD pathogenesis by paying attention to the influence of immunomodulatory treatment on the humoral response. Methods A total of 71 consecutive outpatients with CD, 67 with ulcerative colitis (UC), and 121 healthy controls were analyzed for serum IgA and IgG to C. difficile toxins A and B. Results IgA levels were similar in all study groups. IgG to toxin A was increased similarly in CD and UC ( P = 0.02 for both). In contrast, IgG to toxin B was elevated only in CD patients not receiving disease‐modifying anti‐inflammatory bowel disease drugs (DMAID) ( n = 16) ( P = 0.0001), while the CD medication subgroup ( n = 47) had a level similar to healthy controls. The UC results were not influenced by DMAID treatment. Conclusion Our findings add support to the idea of a disturbed interaction between intestinal cells and the microbiota being part of the CD disease mechanism. An abnormal immune response to C. difficile toxin B may be a critical component of this interaction.