Identification of a novel bacterial sequence associated with Crohn's disease

Evolving Inflammatory Bowel Disease Treatment Paradigms: Top-Down Versus Step-Up

“…[19][20][21][22][23][24] These panels include antibodies directed at several microbial antigens including oligomannan (anti-Saccharomyces cerevisiae or ASCA), Escherichia coli outer membrane porin C (anti-OmpC), flagellin (anti-CBir1), antilaminaribioside (ALCA), antimannobioside (AMCA), antichitobioside (ACCA), antichitin (anti-C), and antilaminarin (anti-L). 21,[25][26][27][28][29][30] The clinical utility of these panels is an area of ongoing interest, but their greatest potential may lie in their predictive capacity (for a more detailed review see the article by Rubin in this issue).…”

Inflammatory bowel disease: autoimmune or immune-mediated pathogenesis?

“…The previously discussed ASCA in CD patients probably reflect the same type of broad anti-microbial reactivity associated with IBD (McKenzie et al, 1990;Giaffer et al, 1992). More recently, novel gut bacterial antigens have been reported in association with IBD, including the Pseudomonas fluorescens-associated sequence I2, the outer membrane porin C of E. coli (OmpC), and bacterial flagellins, towards which CD patients develop significantly higher antibody titers than UC or control subjects (Sutton et al, 2000;Landers et al, 2002;Lodes et al, 2004). Interestingly, it has been suggested that the higher the antibody responses against bacteria and more numerous the antigens against which they react, the more likely it is that CD patients will experience a more severe clinical course, as indicated by a greater frequency of strictures, perforations, and surgical interventions (Mow et al, 2004).…”

Mycobacterium avium subsp paratuberculosis y enfermedad de Crohn: evidencias de una zoonosis

“…Un factor que hace compleja la asociación causal con tales microorganismos, es la signifi cativa modifi cación que presenta la microbiota comensal intestinal de pacientes con EC respecto de personas sanas, situación que puede contribuir a la severidad de la enfermedad y determinar el éxito del tratamiento 20,[23][24][25][26] .…”

“…3. Pese a que varios agentes biológicos podrían estar involucrados en la etiología de EC, MAP se distingue por la generación de una enfermedad crónica mediante la inducción y mantención de una infl amación basada en la respuesta inmune celular, en un rango de distintos tipos histológicos y en diferentes hospederos, incluyendo a los primates 25,27,29 .…”