J Bidwell1, L Keen1, G Gallagher2, R Kimberly3, T Huizinga4, MF McDermott5, J Oksenberg6, J McNicholl7, F Pociot8, C Hardt9 and S D’Alfonso10 Department of Pathology and Microbiology, University of Bristol, Homoeopathic Hospital Site, Cotham, Bristol BS6 6JU, UK; 2University of Glasgow Department of Surgery, Queen Elizabeth Building, Glasgow Royal Infirmary, Glasgow G31 2ER, Scotland, UK; Division of Clinical Immunology and Rheumatology, Tinsley Harrison Tower, Room 429, University of Alabama at Birmingham, 1900 University Boulevard, Birmingham, Alabama 35294-0006, USA; Leiden University Medical Center, Department of Rheumatology, C4-R, PO Box 9600, 2300 RC Leiden, The Netherlands; 5Medical Unit, St. Bartholomew’s and the Royal London Hospital School of Medicine and Dentistry, Whitechapel, London E1 1BB, UK; Department of Neurology, University of California San Francisco, 513 Parnassus Avenue, San Francisco, California 94143-0435, USA; Immunology, DASTLR, NCID, CDC MS A25, 1600 Clifton Road NE, Atlanta, Georgia 30333, USA; 8Steno Diabetes Center, Niels Steensensvej 2, DK-2820 Gentofte, Denmark; Institut für Humangenetik, Universitätsklinikum Essen, Hufelandstr. 55, 45122 Essen, Germany; Dipartimento Scienze Mediche, Via Solaroli 17, 28100 Novara, Italy

Cytokine gene polymorphism in human disease: on-line databases, Supplement 1

Ulcerative colitis (UC) and Crohn's disease (CD) [inflammatory bowel disease (IBD)] are both characterized by an exaggerated immune response at the gut associated lymphoreticular tissue level. Such an abnormal and dysregulated immune response may be directed against luminal and/or enteric bacterial antigens, as also supported by murine models of inflammatory bowel disease (IBD) caused by organisms such as Citrobacter rodentium and Helicobacter hepaticus. Bacterial endotoxins or lipopolysaccharides (LPS) have been detected in the plasma of IBD patients and an abnormal microflora and/or an increased permeability of the intestinal mucosa have been invoked as cofactors responsible for endotoxemia. At the same time, the evidence that phagocytosis and killing exerted by polymorphonuclear cells and monocytes and the T-cell dependent antibacterial activity are decreased in IBD patients may also explain the origin of LPS in these diseases. In IBD, pro-inflammatory cytokines and chemokines have been detected in elevated amounts in mucosal tissue and/or in peripheral blood, thus suggesting a monocyte/macrophage stimulation by enteric bacteria and/or their constituents (e.g. LPS). On these grounds, in experimental models and in human IBD, anti-cytokine monoclonal antibodies and interleukin receptor antagonists are under investigation for their capacity to neutralize the noxious effects of immune mediators. Finally, the administration of lactobacilli is beneficial in human IBD and, in murine colitis, this treatment leads to a normalization of intestinal flora, reducing the number of colonic mucosal adherent and translocated bacteria.

https://journals.sagepub.com/doi/pdf/10.1177/09680519000060030101

Enteric bacteria, lipopolysaccharides and related cytokines in inflammatory bowel disease: biological and clinical significance.

Crohn's disease (CD) and ulcerative colitis (UC), also known as inflammatory bowel diseases (IBD), are characterized by chronic inflammation of the gastrointestinal tract. IBD is among the few complex diseases for which several genomic regions and specific genes have been identified and confirmed in multiple replication studies. We will review the different loci implicated in disease risk in the context of three proposed mechanisms leading to chronic inflammation of the gut mucosa: 1) deregulation of the innate immune response to enteric microflora or pathogens; 2) increased permeability across the epithelial barrier; and 3) defective regulation of the adaptive immune system. As our knowledge of genetic variation, analytical approaches and technology improves, additional genetic risk factors are expected to be identified. With the identification of novel risk variants, additional pathophysiological mechanisms are likely to emerge. The resulting discoveries will further our molecular understanding of IBD, potentially leading to improved disease classification and rational drug design. Moreover, these approaches and tools can be applied in the context of variable drug response with the goal of providing more personalized clinical management of patients with IBD.

https://www.tandfonline.com/doi/pdf/10.1080/07853890701197615

Molecular pathogenesis of inflammatory bowel disease: genotypes, phenotypes and personalized medicine.

Several authors have described an association between celiac disease (CD) and ulcerative colitis (UC), but this has not yet been established. The aim of our study was to examine the frequency of antigliadin antibodies (A G A ), antireticulin antibodies (A RA) and antiendomysium (AEM ) antibodies in the sera of patients with UC (n = 50), and to evaluate their correlation with clinical variables. Sixteen patients with irritable bowel syndrome (IBS) and 37 healthy individuals served as controls. An enzyme-linked immunosorbent assay was used for the detection of IgAand IgG-type AG A. IgG-type A R A were deter­ mined by an indirect immunofluorescence assay (IIF) using rat kidney, liver, and stomach as antigen sub­ strates. IgA-type AEM antibodies were measured by IIF, using cryostat sections from human umbilical cord. Seventeen of the 50 patients with UC (34%) were posi­ tive for IgAor/and IgG-type AG A. There was no cor­ relation between the presence of A G A and the duration or extent o f the disease, or disease activity. However, 5 patients with both IgAand IgG-types of A G A had extensive colitis. Only 2 controls (4%) were positive for IgG-AGA. A R A and AEM were not detected in any individuals studied. Since the A R A and AEM test re­ sults were negative, we conclude that none of the UC patients in this series had CD.

Inflammatory bowel disease: an immunogenetic study

Background: Antibodies to Saccharomyces cerevisiae (ASCA) have been described as specific markers for Crohn disease (CD). The reason for this disease specific generation of antibodies is not clear. Therefore, a family study was performed to evaluate whether the antibody production was due to genetic or environmental factors. Methods: Seventy-one patients with CD, 25 patients with ulcerative colitis (UC), their 282 first-degree relatives, and 32 spouses were included. As controls, 43 sera from healthy persons and 69 sera from patients with various autoimmune disorders were tested for ASCA by indirect immunofluorescence and ELISA. Results: ASCA were detected in 68% of the patients with CD and in none of the controls, UC patients included. Forty-eight (25%) first-degree relatives ofpatients with CD were ASCA-positive. ASCA status of relatives was not related to the fact whether these persons lived in the same household with the patients or not. However, one of the spouses of CD patients (4%) was found to be ...

Anti-Saccharomyces cerevisiae antibodies in inflammatory bowel disease: a family study.

Background: When investigating susceptibility to inflammatory bowel disease (IBD), a multifactorial disorder with a genetic predisposition, polymorphisms of molecules with immunoregulatory function are of potential interest This is the first time that the polymorphisms of HLA-DR and -DQ, tumour necrosis factor (TNF), E-selectin (CD62E), L-selectin (CD62L), and intercellular adhesion molecule 1 (ICAM-1, CD54) were determined in Estonians, a population with a low IBD incidence rate, and their occurrence investigated in subgroups of a total of 53 IBD patients Methods: The reverse hybridization principle and sequence specific primers were used for HLA genotyping To analyse the TNF and adhesion molecule polymorphisms, the polymerase chain reaction with subsequent restriction fragment length polymorphism or single-strand conformation polymorphism method was used Results: In the subgroup of antineutrophil cytoplasmic antibody (ANCA)-positive ulcerative colitis (UC) patients we found a higher frequency of the

Polymorphisms in tumour necrosis factor and adhesion molecule genes in patients with inflammatory bowel disease: associations with HLA-DR and -DQ alleles and subclinical markers.

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Polymorphisms in tumour necrosis factor and adhesion molecule genes in patients with inflammatory bowel disease: associations with HLA-DR and -DQ alleles and subclinical markers.