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PubMed2006

Critical comment: analyzing the effect of novel therapies on cytokine expression in inflammatory bowel disease: do cytokine levels reflect clinical response?

Over the past several years, research in the field of cytokine production and function has become indispensable to understand the immunopathology of chronic intestinal inflammation. Thereupon, clinical studies analyzing cytokine production have generated a tremendous amount of data. In patients with inflammatory bowel disease, several studies examined pro-inflammatory cytokines in gut tissue and plasma, but a clear interpretation of the results with respect to disease activity or therapeutic response has been hampered by patient- and sample-related pitfalls.

Biomarkers↗
PubMed2001

Natural antibodies to nematode biotinyl-enzymes in human sera.

Biotinyl-enzymes are conservative molecules present in helminths, as well as in other animals, bacteria and plants. They have recently been found to be antigenic in mice, and a potential source of cross-reactivity among helminths. This study investigated the presence in human sera of antibodies reactive with biotinyl-enzymes from the nematodes Anisakis simplex, Toxocara canis and Ascaris suum. Biotinyl-enzymes from all these nematodes were recognized by IgG1 antibodies in sera from healthy subjects and from Anisakis-free patients infected with other parasites. Interestingly, IgE antibodies reactive with Anisakis simplex biotinyl-enzymes were present in about one third of the sera from Anisakis-free patients infected with other parasites. Our results also demonstrate that the anti-BE IgG1 and IgE antibodies present in the sera of Anisakis-free subjects are cross-reactive among helminths. We conclude that biotinyl-enzymes from nematodes are recognized by natural human antibodies, although Anisakis biotinyl-enzymes do not seem to be the cause of sensitization. Since sera from the Anisakis-free population also present these antibodies, as-yet unidentified factors (dietary components, intestinal inflammation and/or the presence of parasites) may contribute to the induction of anti-BE antibody background.

Adolescent↗
PubMed2006

Identification of genetic loci for basal cell nevus syndrome and inflammatory bowel disease in a single large pedigree.

Basal Cell Nevus Syndrome (BCNS) is an autosomal dominant disease. PTCH1 gene mutations have been found responsible in many but not all pedigrees. Inflammatory Bowel Disease (IBD) is a complex genetic disorder, disproportionate in Ashkenazim, and characterized by chronic intestinal inflammation. We revisited a large Ashkenazim pedigree, first reported in 1968, with multiple diagnoses of BCNS and IBD, and with a common genetic cause for both disorders proposed. We expanded the pedigree to four generations and performed a genome-wide linkage study for BCNS and IBD traits. Twelve members with BCNS, seven with IBD, five with both diagnoses and eight unaffected were genotyped. Both non-parametric (GENEHUNTER 2.1) and parametric (FASTLINK) linkage analyses were performed and a validation through simulation was performed. BCNS linked to chromosome 9q22 (D9S1120) just proximal to the PTCH1 gene (NPL=3.26, P=0.003; parametric two-point LOD=2.4, parametric multipoint LOD=3.7). Novel IBD linkage evidence was observed at chromosome 1p13 (D1S420, NPL 3.92, P=0.0047; parametric two-point LOD=1.9). Linkage evidence was also observed to previously reported IBD loci on 4q, (D4S2623, NPL 3.02, P=0.012; parametric two-point LOD=2.15), 10q23 (D10S1225 near DLG5, NPL 3.33, P=0.0085; parametric two-point LOD=1.3), 12 overlapping the IBD2 locus (D12S313, NPL 2.6, P=0.018; parametric two-point LOD=1.52), and 7q (D7S510 and D7S3046, NPL 4.06, P=0.0035; parametric two-point LOD=2.18). In this pedigree affected by both BCNS and IBD, the two traits and their respective candidate genetic loci segregate independently; BCNS maps to the PTCH1 gene and IBD maps to several candidate regions, mostly overlapping previously observed IBD loci.

Basal Cell Nevus Syndrome↗
PubMed2004

Adsorptive granulocyte and monocyte apheresis for refractory Crohn's disease: an open multicenter prospective study.

BACKGROUND: Active Crohn's disease (CD) is often associated with elevated levels of platelets, granulocytes, and monocytes that are activated and resistant to apoptosis. The level of neutrophils in the intestinal mucosa has been quantitatively related to the severity of intestinal inflammation in CD. We postulated that patients with CD that is refractory to conventional medications might respond to a reduction of granulocytes and monocytes by adsorptive apheresis. METHODS: Twenty-one patients with a CD activity index (CDAI) of 200-399 and unresponsive to standard medication, which included nutritional intervention, received granulocyte and monocyte adsorptive apheresis (GCAP) as an adjunct to their ongoing medication. GCAP was performed with an Adacolumn, which adsorbs granulocytes, monocytes, and a small fraction of lymphocytes (FcgammaR and complement receptor-bearing leucocytes). Patients received one GCAP session/week for 5 consecutive weeks. CDAI, International Organization for the Study of Inflammatory Bowel Disease (IOIBD), and IBD questionnaire (IBDQ) scores were evaluated. RESULTS: During the initial conventional/nutritional therapy, no significant improvement was seen in any patient. However, at week 7 of GCAP therapy, significant improvements in CDAI, IOIBD, and IBDQ scores were observed. The CDAI, IOIBD, and IBDQ scores before GCAP were 275.6+/-54.2, 3.4+/-1.4, and 152+/-22, respectively. The corresponding values after GCAP were 214.8+/-89.2 (P=0.0005), 2.54+/-1.5 (P=0.0224), and 165+/-29 (P=0.0327), respectively. CONCLUSIONS: GCAP could be effective for inducing remission and improving quality of life in patients with active CD that is refractory to conventional therapy.

Adolescent↗
PubMed1999

Two cases of inflammatory bowel disease with multiple myeloma.

A significant increase has been reported in reticuloendothelial neoplasms in patients with inflammatory bowel diseases. We present two rare cases of multiple myeloma in patients with inflammatory bowel diseases. One was in a 58-year-old woman with ulcerative colitis, and the other was in a 59-year old woman with Crohn's disease. In both patients, multiple myeloma occurred during long-term observation of inflammatory bowel disease and during the inactive stage of intestinal inflammation. The multiple myeloma appeared to have resulted from monoclonal gammopathy of undertermined significance in both patients, and was diagnosed by characteristic serum and bone marrow findings. Our findings suggested that multiple myeloma should be particularly considered in women of middle or advanced age with ulcerative colitis or Crohn's colitis and serum monoclonal gammopathy.

Female↗
PubMed2006

An inverse correlation of human peripheral blood regulatory T cell frequency with the disease activity of ulcerative colitis.

Evidence suggests that CD4+CD25+ regulatory T cells play a crucial role in the suppression of intestinal inflammation. However, their role in the suppression of inflammatory bowel disease has not yet been addressed. We examined the proportion of regulatory T cells in inflammatory bowel disease. First, we isolated CD4+CD45RO+CD25+ T cells from the peripheral blood of healthy persons and showed that these cells suppressed T cell proliferation profoundly and expressed FoxP3 abundantly, revealing that they are regulatory cells. Then the proportion of CD45RO+CD25+ in peripheral blood CD4+ T cells was analyzed in patients and healthy controls by flow cytometry. CD4+CD45RO+CD25+ T cell frequency was significantly lower in active ulcerative colitis than in the control and inactive ulcerative colitis. CD4+CD45RO+CD25+ T cell frequency was inversely correlated with the clinical and endoscopic severity of ulcerative colitis. These results suggest that a deficiency of regulatory T cells is associated with the progression of ulcerative colitis.

Adolescent↗
PubMed1988

Periosteal new bone formation and disseminated granulomatosis in a patient with Crohn's disease.

In a 20-year-old man, a proliferative periosteal new bone growth developed over the left forearm. Crohn's disease had been diagnosed the year before. Bone biopsy demonstrated granuloma formation. Biopsy specimens of skin lesions demonstrated granulomas as well. Bowel studies indicated active small intestinal inflammation with fistula formation. Despite the superficial resemblance to hypertrophic osteoarthropathy, it is believed that this case represents Crohn's disease with disseminated granulomatosis involving skin and periosteum.

Adult↗
PubMed1991

Neutrophil dysfunction in glycogen storage disease Ib: association with Crohn's-like colitis.

Two cases of patients with Crohn's-like colitis and glycogen storage disease Ib have been reported previously. In the current report, chronic inflammatory bowel disease that developed in another adolescent with this glycogenosis is described, thereby corroborating the association. The neutrophil dysfunction observed in glycogen storage disease Ib is the most likely predisposing factor. Neutrophil function was investigated in our patient in an attempt to shed light on the pathogenesis of his intestinal inflammation. The patient displayed reduced neutrophil chemotaxis to zymosan-activated serum, N-formyl-methionine-phenylalanine, and Escherichia coli bacteria-derived factor and reduced intracellular killing of Staphylococcus aureus 502A. Others have found this defective bacteriocidal activity to be caused by impaired oxidative metabolism. The recent recognition of chronic inflammatory bowel disease in glycogen storage disease Ib, as well as in chronic granulomatous disease, suggests that further study of respiratory burst activity of neutrophils in Crohn's disease is warranted.

Adolescent↗
PubMed1992

Soluble interleukin 2 and CD8 and CD4 receptors in inflammatory bowel disease.

Serum levels of soluble interleukin 2 receptor (sIL-2R) have been proposed as a clinical marker of inflammatory bowel disease. The source of sIL-2R in patients with Crohn's disease and ulcerative colitis is unknown, and other soluble receptors have not been investigated. In the present study, sIL-2R and soluble CD8 and CD4 levels were measured in plasma and culture supernatants of peripheral blood and intestinal mucosal mononuclear cells from patients with inflammatory bowel disease, surgical controls, and healthy subjects. Level of plasma sIL-2R was significantly higher in patients with Crohn's disease and ulcerative colitis than in healthy volunteers. Intestinal cells always produced more sIL-2R than peripheral cells. Spontaneous sIL-2R production by mucosal cells was significantly elevated in Crohn's disease but not in ulcerative colitis supernatants compared with levels of surgical controls. Soluble CD8 and CD4 were poor indicators of systemic or mucosal immunity. A positive correlation was found between plasma sIL-2R and spontaneous production by intestinal cells of patients with Crohn's disease and surgical control patients, whereas ulcerative colitis plasma sIL-2R correlated with spontaneous production by peripheral cells. The association of plasma or spontaneous sIL-2R levels with the degree of intestinal inflammation was weak, and there was a wide overlap with control values. Therefore, caution should be used before considering sIL-2R an accurate marker of inflammatory bowel disease activity.

Aged↗
PubMed1994

Eicosanoid production by a differentiated canine colonic epithelial cell line, VNCC.

BACKGROUND/AIMS: The lack of pure, proliferative, but not transformed intestinal epithelial cells has impeded progress in understanding their role in chronic intestinal inflammation. To clarify that role, the present study characterized the epithelial cell line VNCC, derived from normal adult dog distal colon. METHODS: Cells were cultured on plastic and permeable supports for analysis of eicosanoid production (by radioimmunoassay and high-performance liquid chromatography) and transport characteristics (by Ussing chamber short-circuit determinations). RESULTS: In culture, VNCC formed confluent monolayers and domes, suggesting formation of tight junctions and active solute absorption. When cultured on permeable supports, VNCC developed modest, but variable, transepithelial resistances (563 +/- 94 omega/cm2) with a spontaneous short-circuit current of 5.0 +/- 0.4 microA/cm2. Forskolin caused a prolonged increase in the short-circuit current, inhibited by amiloride but not bumetanide, suggesting that VNCC display 5'-cyclic adenosine monophosphate-stimulated sodium absorption. VNCC incubated with arachidonic acid released a variety of eicosanoids including 6-keto-prostaglandin (PG)F1 alpha, PGE2, thromboxane B2, and PGF2 alpha, but no hydroxyarachidonate metabolites. Bradykinin stimulated VNCC eicosanoid release. CONCLUSIONS: The ability of VNCC to divide and differentiate in culture, to form polarized monolayers capable of active sodium absorption, and to respond to inflammatory mediators with eicosanoid release makes them a unique tool for the study of the interactions of inflammation on colonocyte function.

Animals↗
PubMed1995

Anti-inflammatory effects of CGP 47969A, a novel inhibitor of proinflammatory cytokine synthesis, in rabbit immune colitis.

BACKGROUND & AIMS: Proinflammatory cytokines such as interleukin (IL) 1, IL-8, and tumor necrosis factor (TNF) have been implicated as primary mediators of intestinal inflammation. The aim of the present study was to determine the effects of a novel cytokine antagonist (CGP 47969A) in a rabbit model of acute colitis. METHODS: Colitis was induced using the formalin-immune complex technique. Animals were pretreated intrarectally with CGP 47969A (30, 10, or 3 mg/kg), hydrocortisone (0.8 mg/kg), or vehicle (4 mL saline) 2 hours before the induction of colitis and twice daily thereafter until death 48 hours after the induction of colitis. The severity of inflammation of colonic tissue was assessed using histological analysis and myeloperoxidase activity assay, and IL-1 alpha, IL-8, TNF-alpha, and IL-1 receptor antagonist levels were determined. RESULTS: Compared with vehicle, CGP 47969A (10 mg/kg) significantly reduced the acute inflammatory index by 58%, edema by 67%, necrosis by 99%, and myeloperoxidase activity by 49% (all P < 0.02) with efficacy similar to that of steroids. These effects were associated with a significant inhibition of colonic IL-1 alpha and IL-8 by 56% and 90%, respectively (p < 0.01). CONCLUSIONS: Administration of CGP 47969A reduces inflammation and tissue damage in rabbit immune complex colitis through mechanisms involving the inhibition of mucosal proinflammatory cytokines.

Animals↗
PubMed1995

Toxicological studies on ratanjyot oil.

Ratanjyot (Jatropha curcas) grows wild in many parts of India and Brazil. Experimental studies on the toxicity of its oil are scarce despite its use as a cathartic purgative, for treatment of many ailments in human medicine and in industrial applications. This study aims to provide data on its toxicity. The proximate composition of the kernels and physicochemical characteristics of its oil were determined. The kernels constitute 62% of the seed and contain 52% oil, which is reported to contain phorbol esters. A toxic fraction (2.4%) containing the phorbol esters was isolated from the oil. The acute oral LD50 of the oil was found to be 6 ml/kg body weight in rats. The oil caused severe diarrhoea and gastro-intestinal inflammation. The isolated toxic fraction, when applied to the skin of rabbits and rats, produced a severely irritant reaction followed by necrosis; in mice, this fraction had a dermally toxic and lethal effect. The oil and the toxic fraction at 25 and 1 mg respectively in 10 ml saline showed haemolytic activity, disrupting red blood cells. Detoxification or complete removal of the potent toxins present in ratanjyot oil is essential before its use in industrial applications or in human medicine can be considered.

Administration, Oral↗
PubMed1994

Hypercarotenemia and transaminitis in female adolescents with eating disorders: a prospective, controlled study.

PURPOSE: Hypercarotenemia and transaminitis are reported as laboratory features of anorexia nervosa. However, the specificity and sensitivity of an elevation in serum carotene and transaminase are not known. Therefore, a prospective study was undertaken to determine the clinical utility of these serum markers. METHODS: Serum carotene was measured in 46 female adolescents between 13 years and 18 years of age (21 anorexia nervosa, 17 bulimia nervosa, 8 unclassified eating disorders). Findings were compared to levels of carotene in serum samples obtained from similarly aged females with either chronic inflammatory bowel disease (22 Crohn disease, 11 ulcerative colitis) or acute medical symptoms not associated with undernutrition or intestinal inflammation (N = 26), and 21 children of either sex with dyspeptic symptoms. RESULTS: Serum carotene was elevated in 6/46 (13.0%) females with eating disorders compared with only 2/80 (2.5%) children in the three comparison groups (p < 0.01). Hypercarotenemia was present in 4/21 girls with anorexia nervosa compared with 0/17 females with bulimia nervosa (p = 0.11). Transaminitis was present in 38.5% (AST) and 7.7% (ALT) of eating disorder patients. Liver enzyme abnormalities, however, did not correlate with hypercarotenemia. Transaminitis was also not specific for eating disorders since transaminitis was observed with comparable frequency in the three comparison groups. CONCLUSIONS: These findings confirm that hypercarotenemia is a laboratory feature in some subjects with eating disorders, in particular, anorexia nervosa. The low sensitivity (13.0%) does not provide justification for its use as a screening test. However, in complicated diagnostic settings a serum carotene determination could prove useful because the specificity (97.5%), positive predictive value (75.0%), and negative predictive value (66.1%) of an elevated carotene were high. These data also show that elevated carotene levels are not associated with hepatic abnormalities. Although transaminitis is reported as a laboratory feature of eating disorders, the prevalence of such abnormalities in this study was not higher than in age-matched comparison groups.

Adolescent↗
PubMed1995

Hapten-induced chronic colitis in the rat: alternatives to trinitrobenzene sulfonic acid.

Hapten-induced colitis is a widely used model for the study of the intestinal inflammation and for the testing of novel therapies. However, the hapten utilized in this model, trinitrobenzene sulfonic acid, is difficult to obtain in some countries. We therefore compared this hapten to two structurally related haptens to determine if they could be substituted for trinitrobenzene sulfonic acid in terms of inducing chronic colitis in the rat. Rats received one of the three haptens intracolonically, and the severity of colonic inflammation was assessed 3 and 14 days later. Dinitrobenzene sulfonic acid produced colonic inflammation and ulceration that was indistinguishable from that induced by trinitrobenzene sulfonic acid at both time points. On the other hand, dinitrochlorobenzene produced acute colitis (3 days postadministration), but by Day 14 this inflammation had subsided. Dinitrobenzene sulfonic acid and trinitrobenzene sulfonic acid produced comparable levels of granulocyte infiltration into the colon (as measured by tissue myeloperoxidase activity and histology) at both time points. These studies suggest that for studies of up to at least 2 weeks in duration, dinitrobenzene sulfonic acid and trinitrobenzene sulfonic acid produce comparable levels of colonic inflammation. Dinitrobenzene sulfonic acid therefore offers a useful and less expensive alternative to trinitrobenzene sulfonic acid.

Animals↗
PubMed2005

Spondyloarthritis: update on pathogenesis and management.

A great deal of progress has occurred in the past few years in elucidating the causes and designing new treatments for ankylosing spondylitis and other types of spondyloarthritis. In addition to the human leukocyte antigen (HLA)-B27 and other major histocompatibility complex (MHC) genes, chromosomal regions and genes elsewhere in the genome are being implicated both in disease susceptibility and severity. The various ways HLA-B27 may function in causing spondyloarthritis now are better understood to encompass not only antigen presentation but also other mechanisms, possibly all being operative in pathogenesis (misfolding of the HLA-B27 molecule, impaired intracellular killing of bacteria, and HLA-B27 itself serving as an autoantigen). Specific enteric and sexually acquired infections can trigger reactive arthritis, though no specific microbe has been identified in other forms of spondyloarthritis. Intestinal inflammation with impairment of the gut:blood barrier may be operative in driving ankylosing spondylitis and enteropathic arthritis. A number of treatments have been tried in spondyloarthritis, including older agents such as methotrexate and sulfasalazine but also newer drugs such as pamindronate. The recent introduction of tumor necrosis factor (TNF) blockers in the treatment of spondyloarthritis has offered the most hope in not only relieving symptoms and signs of both peripheral arthritis and enthesitis but also spinal disease, which often has been refractory to other agents. Their high cost and considerable side effect profile, however, have necessitated the establishment of guidelines for their use in these diseases in order to target the patient in whom they are likely to have the most benefit.

Anti-Bacterial Agents↗
PubMed2006

n-Butyrate inhibits Jun NH(2)-terminal kinase activation and cytokine transcription in mast cells.

Mast cells are well known to contribute to type I allergic conditions but only recently have been brought in association with chronic relapsing/remitting autoimmune diseases such as celiac disease and ulcerative colitis. Since the bacterial metabolite n-butyrate is considered to counteract intestinal inflammation we investigated the effects of this short chain fatty acid on mast cell activation. Using RNAse protection assays and reporter gene technology we show that n-butyrate downregulates TNF-alpha transcription. This correlates with an impaired activation of the Jun NH(2)-terminal kinase (JNK) but not other MAP kinases such as ERK and p38 that are largely unaffected by n-butyrate. As a consequence, we observed a decreased nuclear activity of AP-1 and NF-AT transcription factors. These results indicate that n-butyrate inhibits critical inflammatory mediators in mast cells by relatively selectively targeting the JNK signalling.

Animals↗
PubMed2004

Specificities of inflammatory bowel disease in childhood.

In parallel with overall population trends, the incidence of paediatric ulcerative colitis (UC) has remained stable, whereas that of paediatric Crohn's disease (CD) has increased in recent decades. Still rare among preschool children, the incidence of both UC and CD rises steadily from middle childhood through adolescence. There is an unexplained preponderance of males with early-onset CD, and an equal gender distribution in paediatric UC. Observations on the familiality of paediatric inflammatory bowel disease (IBD) suggest that genetic susceptibility is particularly important to disease pathogenesis in young patients. In comparison to adult-onset disease, childhood UC is usually extensive but the anatomic localization of paediatric CD varies, as in adults. UC manifests uniformly as bloody diarrhea whereas the symptomatology of paediatric CD is much more diverse. Linear growth impairment frequently complicates chronic intestinal inflammation in paediatric CD. Key contributing factors have been defined; better immunomodulatory therapy and emerging biologic agents will potentially reduce its prevalence.

Adolescent↗
PubMed2005

Eosinophilic gastroenteritis.

Eosinophilic gastroenteritis despite its uncommon occurrence is one of the most important primary eosinophilic gastrointestinal disorders, and most commonly presents with abdominal pain. The terminology is, however, misleading because all levels of the gastrointestinal tract from the esophagus to the rectum may be affected. A history of atopy and allergies is present in 25-75% cases. The heterogeneity in the clinical presentations of EG is determined by the site and depth of eosinophilic infiltration. Eosinophilic intestinal inflammation also occurs secondarily in the gastrointestinal tract in inflammatory bowel disease, autoimmune diseases, as reactions to medications, infections, hypereosinophilia syndrome, and after solid organ transplantation. Recent investigations providing an insight into the pathogenesis of eosinophilic gastroenteritis support a critical role for allergens, eosinophils, Th-2 type cytokines, and eotaxin in mediating eosinophilic inflammation. The diagnosis is confirmed by demonstrating prominent tissue eosinophilia on histopathology. Treatment recommendations based on data extrapolated from retrospective, uncontrolled studies, and expert opinion support the use of restricted diets, corticosteroids, leukotriene receptor antagonists, and mast cell stabilizers. Many unanswered questions remain with regard to the natural history, optimal duration of therapy, safer steroid-sparing long-term treatment agents, and the means of reliable and non-invasive follow-up.

Abdominal Pain↗