571 research outputs found
The Resolution of Intestinal Inflammation: The Peace-Keeper’s Perspective
No full textThe uncontrolled activation of the immune system toward antigens contained in the gut lumen in genetically predisposed subjects is believed to be the leading cause of inflammatory bowel disease (IBD). Two not mutually exclusive hypotheses can explain the pathogenic process leading to IBD. The first and mostly explored hypothesis states that the loss of tolerance toward gut microbiota antigens generates an aberrant inflammatory response that is perpetuated by continuous and unavoidable exposure to the triggering antigens. However, the discovery that the resolution of inflammation is not the mere consequence of clearing inflammatory triggers and diluting pro-inflammatory factors, but rather an active process in which molecular and cellular elements are involved, implies that a defect in the pro-resolving mechanisms might cause chronic inflammation in different immune-mediated diseases, including IBD. Here we review data on pro-resolving and counter-regulatory mechanisms involved in the resolution of inflammation, aiming to identify their possible involvement in the pathogenesis of IBD
Immune system and gut microbiota senescence in elderly IBD patients
No full textIn inflammatory bowel disease (IBD), the loss of immune tolerance against gut microbiota causes chronic inflammation and the progressive accumulation of organ damage in genetically susceptible individuals. In the elderly, IBD is often characterized by a different disease behaviour when compared with paediatric and young adult disease. Besides disease behaviour, another aspect of the multifaceted impact of age on elderly IBD course is increased susceptibility to infections. In this context, age-of-onset-dependent IBD behaviour and clinical course are two major contributors to immune system senescence and change of gut microbiota in older subjects. Here, we review the available literature linking immunosenescence and age-dependent changes in the gut microbiota composition to IBD pathogenesis speculating on their possible implications in disease expression in this age class
Update on the Therapeutic Efficacy of Tregs in IBD: Thumbs up or Thumbs down?
No full textCrohn's disease and ulcerative colitis, the 2 major forms of inflammatory bowel disease (IBD) in humans, arise in genetically predisposed individuals because of an abnormal immune response direct against constituents of the gut flora. Defects in counter-regulatory mechanisms are supposed to amplify and maintain the IBD-associated mucosal inflammation. Therefore, restoring the balance between inflammatory and anti-inflammatory pathways in the gut could contribute to halt the IBD-associated tissue-damaging immune response. Various suppressive T cell (Tregs) subsets have been characterized phenotypically and functionally and over the last decade, there has been enormous effort for optimizing the procedures for the in vitro expansion/generation of these cells for therapeutic purposes. Here we review the mechanisms of action and functional relevance of Tregs in the maintenance of gut inflammation and analyze the available data about the use of these cells in the treatment of IBD patients
Multiple Orocutaneous Extraintestinal Manifestations in Ulcerative Colitis Patient: Complete Response to Ustekinumab
No full textPyostomatitis vegetans (PV) is characterized by exophyticerythematous pustules with superficial erosions of the oral mucosa, while pyoderma gangrenosum (PG) is a rare skin disorder characterized by the development of painful and deeply ulcerated necrotic areas.1 The diagnosis of PV and PG is based on clinical features while histology is unspecific and not always required.2 We report a case of a 73-year-old woman with steroiddependent, long-standing pancolonic ulcerative colitis (UC) previously treated with azathioprine and naïve to biologics. She was admitted to hospital for sepsis (fever 39 °C, white blood cell count 18 000, C-reactive protein >200 mg/dL, procalcitonin 0.75 ng/mL) and moderate UC relapse (partial Mayo score 10, Mayo endoscopic subscore 1) with multiple painful, ulcerated, vegetative and purulent lesions in the oral cavity and skin (leg and sacral regions) (Figure 1). Intravenous (IV) piperacillin-Tazobactam was started and sepsis resolved after 3 days. After dermatological assessment a diagnosis of multiple PG and oral PV was made, IV methylprednisolone 60 mg/d was started. Remission of intestinal symptoms and improvement of orocutaneous lesions were observed until steroid tapering, when orocutaneous lesions worsened. Due to the age of the patient and the recent septic event, anti-Tumor necrosis factor (TNF) treatment was considered not indicated and IV ustekinumab 390 mg was started followed by a maintenance regimen with 90 mg every 8 weeks. Complete healing of the orocutaneous lesions and clinical and biochemical remission (partial Mayo score 0, C-reactive protein normalization, fecal calprotectin [removed]
Common immunologic mechanisms in inflammatory bowel disease and spondylarthropathies
No full textSpondyloarthropathies (SpA) are commonly observed extra-intestinal manifestations of both Crohn's disease (CD) and ulcerative colitis (UC), the two major forms of inflammatory bowel diseases (IBD). However, the immunological link between these two clinical entities is still poorly understood. Several lines of evidence indicate that SpA may originate from the relocation to the joints of the immune process primarily induced in the gut. The transfer of the intestinal inflammatory process into the joints implicates that immune cells activated in the gut-draining lymph nodes can localize, at a certain point of the intestinal disease, either into the gut or into the joints. This is indicated by the overlapping expression of adhesion molecules observed on the surface of intestinal and synovial endothelial cells during inflammation. Moreover bacterial antigens and HLA-B27 expression may be implicated in the reactivation of T cells at the articular level. Finally, accumulating evidence indicates that a T helper 17 cell-mediated immune response may contribute to IBD and IBD-related SpA with a crucial role played by tumor necrosis factor-alpha in CD and to a lesser extent in UC. (C) 2009 The WJG Press and Baishideng. All rights reserved
Plastid Genotyping Reveals the Uniformity of Cytoplasmic Male Sterile-T Maize Cytoplasms
No full textCytoplasmic male-sterile (CMS) lines in maize (Zea mays) have been classified by their response to specific restorer genes into three categories: cms-C, cms-S, and cms-T. A mitochondrial genome representing each of the CMS cytotypes has been sequenced, and male sterility in the cms-S and cms-T cytotypes is linked to chimeric mitochondrial genes. To identify markers for plastid genotyping, we sequenced the plastid genomes of three fertile maize lines (B37, B73, and A188) and the B37 cms-C, cms-S, and cms-T cytoplasmic substitution lines. We found that the plastid genomes of B37 and B73 lines are identical. Furthermore, the fertile and CMS plastid genomes are conserved, differing only by zero to three single-nucleotide polymorphisms (SNPs) in coding regions and by eight to 22 SNPs and 10 to 21 short insertions/deletions in noncoding regions. To gain insight into the origin and transmission of the cms-T trait, we identified three SNPs unique to the cms-T plastids and tested the three diagnostic SNPs in 27 cms-T lines, representing the HA, I, Q, RS, and T male-sterile cytoplasms. We report that each of the tested 27 cms-T group accessions have the same three diagnostic plastid SNPs, indicating a single origin and maternal cotransmission of the cms-T mitochondria and plastids to the seed progeny. Our data exclude exceptional pollen transmission of organelles or multiple horizontal gene transfer events as the source of the mitochondrial urf13-T (unidentified reading frame encoding 13-kD cms-T protein) gene in the cms-T cytoplasms. Plastid genotyping enables a reassessment of the evolutionary relationships of cytoplasms in cultivated maize.Peer reviewe
Erratum: Update on psychological functioning in adults with congenital heart disease: A systematic review (Expert Review of Cardiovascular Therapy (2013) 11(6) (785–791) (10.1586/erc.13.9))
No full textThe correct author affiliations are given below: Edward Callus*1, Emilia Quadri1, Cristian Ricci2, Cristiana Passerini1, Anna Tovo1, Gabriele Pelissero3 and Massimo Chessa11IRCCS Policlinico San Donato, Pediatric and Adult Congenital Heart Centre, Italy 2Fondazione Don C. Gnocchi, Italy 3IRCCS Policlinico San Donato, Scientific Directorate, Italy *Author for correspondence: Tel.: +39 02 527 747 07 [email protected]. © 2013, Informa UK, Ltd. All rights reserved
Molecular actions of 5-aminosalicylic acid: the magic bullet on epidermal growth factor receptor signalling
No full textBuyers' Miscoordination, Entry and Downstream Competition
No full textThis article shows that buyers' coordination failures might prevent entry in an industry with an incumbent firm and a more efficient potential entrant. If there were a single buyer, or if all buyers formed a central purchasing agency, coordination failures would be avoided and efficient entry would always occur. More generally, exclusion is less likely the lower the number of buyers. For any given number of buyers, exclusion is less likely the more fiercely buyers compete in the downstream market. First, intense competition may prevent miscoordination equilibria from arising; second, in cases where miscoordination equilibria still exist, it lowers the maximum price that the incumbent can sustain at such exclusionary equilibria. Copyright (C) The Author(s). Journal compilation (C) Royal Economic Society 2008.
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