The pathogenesis of @entity29 ( @entity29 ) proceeds through stages of initiation, amplification and healing. Abundant clinical and experimental data incriminate luminal bacteria or bacterial products in both the initiation and perpetuation of chronic @entity32 . Macrophage and T-cell activation with accompanying inflammatory cytokine production appears to be an early event. Studies of lymphocyte responsiveness to autologous and heterologous intestinal bacteria have suggested that this activation may result from a breakdown in tolerance to the enteric flora in @entity29 . This lack of tolerance might be due to an imbalance between protective and aggressive commensal luminal bacterial species ( @entity6636 ), a decreased barrier function and/or an @entity73 allowing the access of bacteria to the mucosal immune system and lack of regulatory mediators or cells. There is still controversy over whether the virulence traits of bacteria are expressed broadly or just in a small subset of bacteria. Individual bacterial species within the indigenous flora vary in their capacity to drive @entity32 . In experimental models, some bacteria such as @entity3395 can cause @entity1960 alone when monoassociated in the HLA-B27 transgenic @entity35 model. Others, including Lactobacillus and Bifidobacterium species have no proinflammatory capacity and have been used as probiotics. In @entity1 with @entity29 , systematic approach to this issue is hampered by the limited knowledge of intestinal flora. Adherent-invasive @entity526 are a possible candidate for the onset and/or persistence of @entity32 in @entity1 with @entity30 , since they possess all the virulence factors that allow the bacteria to cross the intestinal barrier, to move to deep tissues, and to continuously activate macrophages. The recent identification of @entity6820 / @entity6820 as a susceptibility gene for @entity30 has provided another link between the immune response to enteric bacteria and the development of @entity32 . @entity6820 / @entity6820 is composed of two caspase recruitment domain (CARD), a @entity377 -binding domain (NBD) and a @entity368 -rich-repeat (LRR) region. The LRR domain of @entity6820 / @entity6820 has binding activity for bacterial peptidoglycans and its deletion stimulates the NF-kappaB pathway. The most frequent variants of @entity6820 / @entity6820 observed in @entity30 tend to cluster in the LRR and its adjacent regions. This suggests that the LRR domain of CD-associated variants is likely to be impaired in its recognition of microbial components. Continuing studies are investigating the pathophysiological mechanisms induced by @entity6820 / @entity6820 variants in the intestinal mucosa.

[Intestinal flora and XXXX ].

@entity1 :: ('9606', 'Species') :: ['patients'] @entity32 :: ('MESH:D007249', 'Disease') :: ['mucosal inflammation', 'intestinal inflammation'] @entity368 :: ('CHEBI:25017', 'Chemical') :: ['leucin'] @entity73 :: ('MESH:D003072', 'Disease') :: ['impaired mucosal clearance'] @entity3395 :: ('821', 'Species') :: ['Bacteroides vulgatus'] @entity377 :: ('CHEBI:36976', 'Chemical') :: ['nucleotide'] @entity6636 :: ('MESH:D064806', 'Disease') :: ['dysbiosis'] @entity29 :: ('MESH:D015212', 'Disease') :: ['inflammatory bowel diseases', 'IBD'] @entity1960 :: ('MESH:D003092', 'Disease') :: ['colitis'] @entity6820 :: ('64127', 'Gene') :: ['CARD15', 'NOD2'] @entity35 :: ('10116', 'Species') :: ['rat'] @entity30 :: ('MESH:D003424', 'Disease') :: ["Crohn's disease"] @entity526 :: ('562', 'Species') :: ['Escherichia coli']
@entity30 :: (MESH:D003424,Disease) :: ['Crohn's disease']
