Hungarian IBD Study Group members are as follows: Peter Fuszek, Orsolya Gemela, Henrik Csaba Horvath, Peter Vargha and Ferenc Szalay (1st Department of Medicine, Semmelweis University, Budapest, Hungary); Zsuzsanna Erdelyi, Gabor Mester, Csaba Molnar and Tunde Pandur (1st Department of Medicine, Csolnoky F. County Hospital, Veszprem, Hungary); Ferenc Nagy and Janos Lonovics (1st Department of Medicine, University of Szeged, Szeged, Hungary); Levente Balint, Pal Demeter, Istvan Dobo and Ferenc Huoranszky (Department of Gastroenterology and Surgery, St. Margit Hospital, Budapest, Hungary); and Laszlo Herszenyi and Annamaria Nemeth (2nd Department of Medicine, Semmelweis University, Budapest, Hungary).
Interaction between seroreactivity to microbial antigens and genetics in Crohn’s disease: is there a role for defensins?
Version of Record online: 7 APR 2008
© 2008 The Authors Journal compilation © 2008 Blackwell Munksgaard
Volume 71, Issue 6, pages 552–559, June 2008
How to Cite
Lakatos, P. L., Altorjay, I., Mándi, Y., Lakatos, L., Tumpek, J., Kovacs, A., Molnar, T., Tulassay, Z., Miheller, P., Palatka, K., Szamosi, T., Fischer, S., Papp, J., the Hungarian IBD Study Group and Papp, M. (2008), Interaction between seroreactivity to microbial antigens and genetics in Crohn’s disease: is there a role for defensins?. Tissue Antigens, 71: 552–559. doi: 10.1111/j.1399-0039.2008.01049.x
- Issue online: 7 APR 2008
- Version of Record online: 7 APR 2008
- Received 14 January 2008; revised 26 February 2008, 9 March 2008; accepted 16 March 2008
- Crohn’s disease;
Antibodies against different microbial epitopes are associated with disease phenotype, may be of diagnostic importance and may reflect a loss of tolerance in Crohn’s disease (CD). Recently, an association was reported between the presence of these antibodies and mutations in pattern receptor genes. Our aim was to investigate whether mutations in various genes other than NOD2/CARD15 or TLR4 associated with CD (NOD1/CARD4, DLG5 and DEFB1) may influence the presence of antibodies against bacterial proteins and carbohydrates in a Hungarian cohort of CD patients. Three hundred and seventy-six well-characterized, unrelated, consecutive CD patients (male/female: 191/185, age at onset: 29.1 ± 12.9 years, duration: 7.9 ± 11.7 years) were investigated. Sera were assayed for anti-Omp, anti-Saccharomyces cerevisiae antibodies (ASCAs) immunoglobulin (Ig) A and IgG, and antibodies against a mannan epitope of S. cerevisiae (gASCA), laminaribioside (ALCA), chitobioside (ACCA), and mannobioside (AMCA). NOD1/CARD4, DLG5 and DEFB1 variants were tested by polymerase chain reaction–restriction fragment length polymorphism, and DEFB1 was genotyped in a subgroup of 160 patients. Detailed clinical phenotypes were determined by reviewing the patients’ medical charts. The carriage of DEFB1 20A variant alleles less frequently led to antiglycan positivity compared with patients without (29.6% vs 46.2%, OR: 0.49, 95% CI: 0.25–0.97), regardless of disease location or behavior. Similar tendency was observed for DEFB1 44G (present: 21.6% vs absent: 10.2%, P = 0.06) and ALCA. A gene or serology dosage effect was not observed. However, no association was found between the DEFB1 G52A, DLG5 R30Q, and NOD1/CARD4 E266K variants and any of the serology markers. We found that variants in human β-defensin 1 gene are inversely associated with antiglycan antibodies, further confirming an important role for innate immunity in the pathogenesis of CD.