Ulcerative Colitis: Desreumaux P

Desreumaux P, Nutten S, Colombel JF. · No affiliation provided · Am J Gastroenterol. · Pubmed #10606287 No free full text.

This publication has no abstract.

Rousseaux C, Desreumaux P. · Laboratoire de Physiopathologie des Maladies Inflammatoires Intestinales, INSERM E114, Hôpital Huriez, Service de Gastroentérologie, 1, place de Verdun, 59000 Lille. · J Soc Biol. · Pubmed #17151549 No free full text.

Abstract: PPARgamma has been recently described as being a gene of susceptibility for Intestinal Bowel Diseases (IBD) as NOD2/CARD15 gene. IBD are pathologies due to an abnormal immune response, in genetically predisposed patients, to the bacteria of the intestinal flora. PPARgamma, known for its significant role in adipogenesis, is strongly expressed by the epithelial cells of the colon mucosa. PPARgamma is implicated in the regulation of inflammation. Indeed, agonists of this nuclear receptor decrease strongly the intensity of inflammation during experimental colitis induced by chemical agents. A deficit of PPARgamma in patients with ulcerative colitis has been highlighted, that could in part explain the acute inflammation. In addition, bacteria, including those of the commensal flora, are able to regulate PPARgamma. Toll Like Receptor-4 (TLR-4), responsible for the recognition of bacterial motif as lipopolysaccharide (LPS), is implicated in PPARgamma regulation and its anti-inflammatory properties. All these arguments make of PPARgamma a very interesting therapeutic target for the treatment of IBD.

Desreumaux P, Ghosh S. · INSERM U795, Lille, France. · Aliment Pharmacol Ther. · Pubmed #16939423 No free full text.

Abstract: The effectiveness of sulfasalazine depends on the splitting of the diazo bond in the molecule by the action of bacteria in the large bowel, releasing the pharmacologically active moiety, 5-aminosalicylic acid. The development of pH-dependent, delayed-release formulations of 5-aminosalicylic acid abolished the toxicity associated with the sulfapyridine part of sulfasalazine. 5-aminosalicylic acid is now believed to act by activating a class of nuclear receptors involved in the control of inflammation, cell proliferation, apoptosis and metabolic function, the gamma form of peroxisome proliferator-activated receptors. These receptors are expressed at particularly high levels in colon epithelial cells, where their expression appears to be at least in part stimulated by gut bacteria. Other drugs known to act via peroxisome proliferator-activated receptor-gamma, such as rosiglitazone and the selective peroxisome proliferator-activated receptor-gamma ligand GW1929, can be displaced from their binding sites on the peroxisome proliferator-activated receptor-gamma molecule by 5-aminosalicylic acid at concentrations of 5-aminosalicylic acid that correspond with the concentrations found in the lumen of ulcerative colitis patients taking oral mesalazine. Genetically engineered heterozygous knockout mice (peroxisome proliferator-activated receptor-gamma+/-) are particularly susceptible to colonic inflammation, and inflammation is more severe in these mice, in response to chemicals that induce experimental colonic ulcers. In these experimental models, 5-aminosalicylic acid is ineffective in peroxisome proliferator-activated receptor-gamma+/- mice. This new insight provides a mechanistic foundation for the possibility that long-term treatment with 5-aminosalicylic acid can reduce the risk of colorectal cancer in patients with ulcerative colitis.

Dubuquoy L, Rousseaux C, Thuru X, Peyrin-Biroulet L, Romano O, Chavatte P, Chamaillard M, Desreumaux P. · INSERM U795 ex E114, Clinique des Maladies de l'Appareil Digestif et de la Nutrition, Hôpital Swynghedauw, rue A Verhaeghe, F-59037 Lille Cedex, France. · Gut. · Pubmed #16905700 No free full text.

Abstract: The peroxisome proliferator activated receptor gamma(PPARgamma) is a nuclear receptor highly expressed in the colon and playing a key role in bacterial induced inflammation. Regulation of colon inflammation by this receptor has been well demonstrated in many experimental models of colitis but also in patients with ulcerative colitis, characterised by impaired expression of PPARgamma confined to their colon epithelial cells. Recent data showing that PPARgamma was the major functional receptor mediating the common aminosalicylate activities in inflammatory bowel diseases (IBD) have also reinforced the roles of this receptor in the control of intestinal inflammation. The aims of this review are to discuss the potential roles of PPARgamma in the physiopathology of IBD, as well as the emerging therapeutic strategies targeting this receptor.

Cheng Y, Desreumaux P. · Institute of Liver Disease, Shanghai University of Traditional Chinese Medicine, No.1200 Cailun Road, Pudong District, Shanghai 201203, China. · World J Gastroenterol. · Pubmed #15637733 links to  free full text

Abstract: Inflammatory bowel disease (IBD) is classically subdivided into ulcerative colitis (UC) and Crohn's disease (CD). Patients with IBD have increased risk for colorectal cancer. Because the pathogenesis of colorectal carcinoma has not been entirely defined yet and there is no ideal treatment for colon cancer, cancer prevention has become increasingly important in patients with IBD. The two adopted methods to prevent the development of colon cancer in clinical practice include the prophylactic colectomy and colonoscopic surveillance. But patients and physicians seldom accept colectomy as a routine preventive method and most patients do not undergo appropriate colonoscopic surveillance. Chemoprevention refers to the use of natural or synthetic chemical agents to reverse, suppress, or to delay the process of carcinogenesis. Chemoprevention is a particularly useful method in the management of patients at high risk for the development of specific cancers based on inborn genetic susceptibility, the presence of cancer-associated disease, or other known risk factors. Prevention of colorectal cancer by administration of chemopreventive agents is one of the most promising options for IBD patients who are at increased risks of the disease. The chemopreventive efficacy of nonsteroidal anti-inflammatory drugs (NSAIDs) against intestinal tumors has been well established. But with reports that NSAIDs aggravated the symptoms of colitis, their sustained use for the purpose of cancer chemoprevention has been relatively contraindicated in IBD patients. Another hopeful candidate chemoprevention drug for IBD patients is 5-aminosalicylic acid (5-ASA), which is well tolerated by most patients and has limited systemic adverse effects, and no gastrointestinal toxicity. 5-ASA lacks the well-known side effects of long-term NSAIDs use. Retrospective correlative studies have suggested that the long-term use of 5-ASA in IBD patients may significantly reduce the risk of development of colorectal cancer. According to the literature, this agent might well satisfy clinical expectations with respect to a safe and effective chemopreventive agent.

Tamboli CP, Caucheteux C, Cortot A, Colombel JF, Desreumaux P. · Service de Gastroentérologie, Hôpital Huriez, CHRU, Lille 59037, France. · Best Pract Res Clin Gastroenterol. · Pubmed #14507590 No free full text.

Abstract: Intestinal bacteria play a key role in inflammatory bowel disease. Probiotics attempt to modify disease by favourably altering bacterial composition, immune status, and inflammation. Until recently, probiotic therapy was considered 'folk' medicine, but there now is emerging interest on the part of the general public and scientific communities in the use of probiotics in human disease. This practical, evidence-based review examines probiotics as therapy for inflammatory bowel disease in humans. There are very few such published randomized clinical trials, but some data exist that possibly show an efficacy of probiotics as maintenance therapy in chronic relapsing pouchitis. Obstacles to providing probiotic therapy include selection of appropriate strains, poorly regulated probiotic quality standardization, processing and human biologic factors which impair probiotic viability, difficulty in maintaining new bacterial populations in the gut, and local product unavailability. Studies have focused on specific inflammatory bowel disease subgroups, limiting general applicability for the practitioner. Basic research highlights the importance of bacteria in these conditions, and the possibility that probiotics will modify physiological parameters. Well-designed, randomized clinical studies are still required to define the role of probiotics as therapeutic agents in inflammatory bowel disease.

Geboes K, Desreumaux P, Jouret A, Ectors N, Rutgeerts P, Colombel JF. · Département de Pathologie et de Gastroentérologie, Hôpital Universitaire, KU Leuven, Belgique. · Gastroenterol Clin Biol. · Pubmed #10592879 No free full text.

This publication has no abstract.

Guidat A, Fleyfel M, Vallet B, Desreumaux P, Levron JC, Gambiez L, Colombel JF, Scherpereel P. · Hôpital Claude Huriez, Département d'Anesthésie Réanimation 2, Lille, France. · Eur J Anaesthesiol. · Pubmed #14690097 No free full text.

Abstract: BACKGROUND AND OBJECTIVE: Inflammation promotes hyperalgesia and increases opioid binding protein (alpha1-acid glycoprotein) inducing increased opioid requirement. To investigate the influence of an acute episode of inflammatory bowel disease in opioid requirement during major abdominal surgery, 17 patients with Crohn's disease, 12 patients with ulcerative colitis and seven patients without any inflammatory process (control group) were prospectively studied. Sufentanil requirements were assessed during surgery. METHODS: Sufentanil administration was adjusted when haemodynamic variables changed more than 20% of preoperative values. In a subgroup of 20 patients (Crohn's disease: 7, ulcerative colitis: 7, control group: 6), plasma concentrations of alpha1-acid glycoprotein and unbound sufentanil were measured. Total plasma clearance of sufentanil was also determined. Data presented as median (25-75 per thousand) were analysed by non-parametric and ANOVA tests. RESULTS: Despite similar surgery duration, intraoperative sufentanil requirements were significantly larger in both the Crohn's disease group (0.9 (0.6-1.6) microg kg(-1) h(-1)) and the ulcerative colitis group (1.1 (0.6-1.7) microg kg(-1) h(-1)) than in the control group (0.5 (0.4-0.5) microg kg(-1) h(-1)). Total plasma clearance of sufentanil was larger in patients with inflammatory bowel disease than in the control group. The plasma alpha1-acid glycoprotein concentration was increased in the inflammatory bowel disease group. However, the free fraction of sufentanil was similar in all three groups. The largest sufentanil consumption in patients with inflammatory bowel disease was observed during time of pain stimulation in the area of referred hyperalgesia from the affected viscus. In the control group, the sufentanil requirement was constant throughout surgery. CONCLUSION: Inflammatory bowel disease increases opioid requirement during major abdominal surgery.

Louvet B, Buisine MP, Desreumaux P, Tremaine WJ, Aubert JP, Porchet N, Capron M, Cortot A, Colombel JF, Sandborn WJ. · Laboratoire de recherche sur les MICI (CRI 4U004B), Centre Hospitalier Universitaire (CHU), Lille, France. · Inflamm Bowel Dis. · Pubmed #10453373 No free full text.

Abstract: Our goal was to determine the effect of transdermal nicotine on cytokine and mucin gene transcription in ulcerative colitis (UC). Sixty-four nonsmoking patients with active UC were randomly assigned to transdermal nicotine (maximum dose 22 mg/day) or placebo for 4 weeks. Clinical assessment and colonic mucosal biopsies were obtained at entry and after 4 weeks. Inflammatory and immunoregulatory cytokines were assessed by qualitative reverse transcriptase-polymerase chain reaction (RT-PCR). Based on this initial screen. IL-8 mRNA levels were measured by RT-competitive PCR. MUC1, MUC2, MUC3, MUC4, MUC5AC, MUC5B, and MUC6 mRNA concentrations were measured by quantitative dot blot analysis. Cytokine mRNA expression, except for IL-8, was similar in all patients. IL-8 mRNA levels were significantly decreased in the colonic mucosa of nicotine-treated patients who improved (p = 0.04). IL-8 mRNA values were similar before and after treatment in nonresponding nicotine-treated patients and in all placebo-treated patients. Mucin gene expression was similar in all patient groups. Beneficial effects of transdermal nicotine in active UC may result from decrease of IL-8 expression at the transcriptional level. Transdermal nicotine has no effect on mucin gene transcription.

Karrout Y, Neut C, Wils D, Siepmann F, Deremaux L, Flament MP, Dubreuil L, Desreumaux P, Siepmann J. · College of Pharmacy, JE 2491, Universite Lille Nord de France, 3 rue du Professeur Laguesse, 59006 Lille, France. · Eur J Pharm Sci. · Pubmed #19491034 No free full text.

Abstract: The aim of this study was to prepare and characterize novel types of polymer coated pellets allowing for the site-specific delivery of drugs to the colon. 5-Aminosalicylic acid (5-ASA)-loaded beads were prepared by extrusion-spheronization and coated with different Nutriose:ethylcellulose blends. In vitro drug release from these systems was measured under various conditions, including the exposure to fresh fecal samples from inflammatory bowel disease patients under anaerobic conditions. Nutriose is a starch derivative, which is preferentially degraded by enzymes secreted by the microflora in the colon of Crohn's disease and ulcerative colitis patients. Interestingly, the release of 5-ASA (which is commonly used for the local treatment of inflammatory bowel diseases) could effectively be suppressed upon exposure to release media simulating the conditions in the upper GIT, irrespective of the degree of agitation and presence or absence of enzymes. But as soon as the pellets came into contact with fecal samples of inflammatory bowel disease patients, the release rate significantly increased and the drug was released in a time-controlled manner. Thus, this novel type of colon targeting system is adapted to the pathophysiology of the patient. Furthermore, culture media containing specific colonic bacteria are presented providing an interesting potential as substitutes for fresh fecal samples.

Karrout Y, Neut C, Wils D, Siepmann F, Deremaux L, Desreumaux P, Siepmann J. · College of Pharmacy, JE 2491, University of Lille, 3 rue du Professeur Laguesse, 59006 Lille, France. · Int J Pharm. · Pubmed #19135511 No free full text.

Abstract: The major aim of this work was to optimize the properties of novel polymeric films based on blends of ethylcellulose and Nutriose (a water-soluble, branched dextrin). Such blends were recently shown to be highly promising for the site-specific delivery of drugs to the colon in patients suffering from inflammatory bowel diseases, in particular Crohn's disease and ulcerative colitis. Importantly, and in contrast to various other colon targeting approaches, the system is adapted to the pathophysiological conditions in the disease state. However, it is yet unknown how desired membrane properties, especially water uptake and dry mass loss kinetics as well as mechanical stability can be adjusted to the specific needs of particular drug treatments. Different highly efficient and easy to apply tools were identified altering the membrane's properties, in particular their mechanical resistance required to withstand the shear forces resulting from the motility of the upper GIT and the hydrostatic pressure built up within the devices upon contact with aqueous media. This includes the variation of the Nutriose:ethylcellulose blend ratio and initial plasticizer content. Importantly, Nutriose also exhibits significant pre-biotic activity, normalizing the microflora in the patients' colon, which is of major clinical benefit in the case of inflammatory bowel diseases.

Desreumaux P, Dubuquoy L. · University of Lille 2, Huriez Hospital, Digestive Tract Diseases and Nutrition Department, Lille, France. · Inflamm Bowel Dis. · Pubmed #18798571 No free full text.

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Coste A, Dubuquoy L, Barnouin R, Annicotte JS, Magnier B, Notti M, Corazza N, Antal MC, Metzger D, Desreumaux P, Brunner T, Auwerx J, Schoonjans K. · Institut de Génétique et de Biologie Moléculaire et Cellulaire, CNRS, INSERM, Université Louis Pasteur, Illkirch, and Service des Maladies de l'Appareil Digestif et de la Nutrition, Hôpital Huriez, Lille, France. · Proc Natl Acad Sci U S A. · Pubmed #17670946 links to  free full text

Abstract: Liver receptor homolog-1 (LRH-1) is a nuclear receptor involved in intestinal lipid homeostasis and cell proliferation. Here we show that haploinsufficiency of LRH-1 predisposes mice to the development of intestinal inflammation. Besides the increased inflammatory response, LRH-1 heterozygous mice exposed to 2,4,6-trinitrobenzene sulfonic acid show lower local corticosterone production as a result of an impaired intestinal expression of the enzymes CYP11A1 and CYP11B1, which control the local synthesis of corticosterone in the intestine. Local glucocorticoid production is strictly enterocyte-dependent because it is robustly reduced in epithelium-specific LRH-1-deficient mice. Consistent with these findings, colon biopsies of patients with Crohn's disease and ulcerative colitis show reduced expression of LRH-1 and genes involved in the production of glucocorticoids. Hence, LRH-1 regulates intestinal immunity in response to immunological stress by triggering local glucocorticoid production. These findings underscore the importance of LRH-1 in the control of intestinal inflammation and the pathogenesis of inflammatory bowel disease.

Malamut G, Cabane C, Dubuquoy L, Malapel M, Dérijard B, Gay J, Tamboli C, Colombel JF, Desreumaux P. · INSERM 0114, Lille, F-59037, France. · Dig Dis Sci. · Pubmed #16838116 No free full text.

Abstract: Involvement of mitogen-activated protein (MAPK) in inflammatory bowel disease (IBD) remains enigmatic. We sought to evaluate the expression and activity of p38 and JNK MAPK in IBD and 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis; and the effects of a p38 inhibitor, SB203580, in TNBS colitis. P38 and JNK were quantified in colonic mucosa of 28 IBD patients and 19 controls and in 77 TNBS or control mice treated or not with SB203580. Colitis severity was assessed by survival, macroscopic and microscopic scoring, and molecular markers. Expression and activity of p38 and JNK were similar in IBD patients and controls and not modified by inflammation. In mice, p38 and JNK expression or activity did not increase following the induction of colitis. SB203580 decreased the p38 activity but displayed no clinical nor biological therapeutic effect. In conclusion, these results minimize the role of p38 and JNK in inflammatory colitis and the interest of p38 as a therapeutic target in IBD.

Philippe D, Chakass D, Thuru X, Zerbib P, Tsicopoulos A, Geboes K, Bulois P, Breisse M, Vorng H, Gay J, Colombel JF, Desreumaux P, Chamaillard M. · INSERM, Lille, France. · Gut. · Pubmed #16299031 links to  free full text

Abstract: BACKGROUND AND AIMS: Recent studies with mu opioid receptor (MOR) deficient mice support a physiological anti-inflammatory effect of MOR at the colon interface. To better understand the potential pharmacological effect of certain opiates in inflammatory bowel diseases (IBD), we (1) evaluated the regulation in vivo and in vitro of human MOR expression by inflammation; and (2) tested the potential anti-inflammatory function of a specific opiate (DALDA) in inflamed and resting human mucosa. PATIENTS AND METHODS: Expression of MOR mRNA and protein was evaluated in healthy and inflamed small bowel and colonic tissues, isolated peripheral blood mononuclear cells and purified monocytes, and CD4+ and CD8+ T cells from healthy donors and IBD patients. The effect of cytokines and nuclear factor kappaB (NFkappaB) activation on MOR expression in lymphocyte T and monocytic human cell lines was assessed. Finally, DALDA induced anti-inflammatory effect was investigated in mucosal explants from controls and IBD patients. RESULTS: MOR was expressed in ileal and colonic enteric neurones as well as in immunocytes such as myeloid cells and CD4+ and CD8+ T cells. Overexpressed in active IBD mucosa, MOR was significantly enhanced by cytokines and repressed by NFkappaB inhibitor in myeloid and lymphocytic cell lines. Furthermore, ex vivo DALDA treatment dampened tumour necrosis factor alpha mRNA expression in the colon of active IBD patients. CONCLUSIONS: Given the increased expression of MOR and the ex vivo beneficial effect of DALDA in active IBD, natural and/or synthetic opioid agonists could help to prevent overt pathological intestinal inflammation.

Godeberge P, Desreumaux P, Slim K, Dupas JL, Marteau P, Beaugerie L, Bouhnik Y, Flourié B, Gambiez L, Reimund JM, Seksik P. · Département médico-chirurgical de pathologie digestive, Institut Mutualiste Montsouris, 75014 Paris. · Gastroenterol Clin Biol. · Pubmed #15672565 No free full text.

This publication has no abstract.

Barbier M, Vidal H, Desreumaux P, Dubuquoy L, Bourreille A, Colombel JF, Cherbut C, Galmiche JP. · Pôle Digestif et CIC-INSERM, CHU Nantes et INRA, 44093 Nantes Cedex 1. · Gastroenterol Clin Biol. · Pubmed #14732844 links to  free full text

Abstract: BACKGROUND: Leptin, a protein with a cytokine-like structure, is produced predominantly by adipocytes. It appears to play a key role in immune responses by increasing the secretion of Th1 and pro-inflammatory cytokines. As fat-wrapping is a characteristic feature of Crohn's disease (CD), and as increased leptin levels have been reported in animal models of intestinal inflammation, this study investigated whether mesenteric adipose tissue could be a source of leptin in human inflammatory bowel disease (IBD). AIM: To quantify the expression of leptin mRNA in mesenteric adipose tissue of patients with CD or ulcerative colitis (UC). METHODS: Specimens were obtained from mesenteric white adipose tissue close to healthy and inflammatory small intestine and/or colon in patients with CD or UC and, for controls, from apparently healthy mesentery of patients operated for carcinoma of the right colon. The expression of leptin mRNA was assessed by reverse transcription-competitive polymerase chain reaction. RESULTS: Leptin mRNA levels were significantly higher in mesenteric adipose tissue of CD and UC patients than in controls (P<0.05). In CD and UC, concentrations were not significantly different in mesenteric fat specimens, whether contiguous to macroscopically normal or grossly abnormal intestine. CONCLUSIONS: This study provides the first evidence of a novel abnormality of the mesentery of patients with IBD. Overexpression of leptin mRNA in mesenteric adipose tissue may contribute to (a) the inflammatory process, (b) enhancement of mesenteric TNF alpha expression in CD (as recently reported), and/or (c) the anorexia frequently reported during flares of IBD.

Dubuquoy L, Jansson EA, Deeb S, Rakotobe S, Karoui M, Colombel JF, Auwerx J, Pettersson S, Desreumaux P. · Equipe Propre INSERM 0114 sur la Physiopathologie des Maladies Inflammatoires Intestinales, Lille, France. · Gastroenterology. · Pubmed #12730867 No free full text.

Abstract: BACKGROUND & AIMS: The peroxisome proliferator-activated receptor gamma (PPAR gamma) has been proposed as a key inhibitor of colitis through attenuation of nuclear factor kappa B (NF-kappa B) activity. In inflammatory bowel disease, activators of NF-kappa B, including the bacterial receptor toll-like receptor (TLR)4, are elevated. We aimed to determine the role of bacteria and their signaling effects on PPAR gamma regulation during inflammatory bowel disease (IBD). METHODS: TLR4-transfected Caco-2 cells, germ-free mice, and mice devoid of functional TLR4 (Lps(d)/Lps(d) mice) were assessed for their expression of PPAR gamma in colonic tissues in the presence or absence of bacteria. This nuclear receptor expression and the polymorphisms of gene also were assessed in patients with Crohn's disease (CD) and ulcerative colitis (UC), 2 inflammatory bowel diseases resulting from an abnormal immune response to bacterial antigens. RESULTS: TLR4-transfected Caco-2 cells showed that the TLR4 signaling pathway elevated PPAR gamma expression and a PPAR gamma-dependent reporter in an I kappa kappa beta dependent fashion. Murine and human intestinal flora induced PPAR gamma expression in colonic epithelial cells of control mice. PPAR gamma expression was significantly higher in the colon of control compared with Lps(d)/Lps(d) mice. Although PPAR gamma levels appeared normal in patients with CD and controls, UC patients displayed a reduced expression of PPAR gamma confined to colonic epithelial cells, without any mutation in the PPAR gamma gene. CONCLUSIONS: These data showed that the commensal intestinal flora affects the expression of PPAR gamma and that PPAR gamma expression is considerably impaired in patients with UC.

Desreumaux P, Colombel JF. · Service des Maladies de l'Appareil Digestif et de la Nutrition, Hôpital Huriez, CHRU, 59037 Lille. · Gastroenterol Clin Biol. · Pubmed #11787387 No free full text.

This publication has no abstract.

Bulois P, Tremaine WJ, Maunoury V, Gambiez L, Hafraoui S, Leteurtre L, Cortot A, Sandborn WJ, Colombel JF, Desreumaux P. · Laboratoire de Recherche des Maladies Inflammatoires Intestinales, CHU Lille, France. · Inflamm Bowel Dis. · Pubmed #10961587 No free full text.

Abstract: BACKGROUND: Mucosal lesions of pouchitis are characterized by a neutrophil infiltrate. Interleukin (IL)-8 is the main mediator involved in neutrophil recruitment and is down-regulated by IL-10. AIM: To look for an imbalance between IL-8 and IL-10 in patients with pouchitis. PATIENTS/METHODS: 18 patients having an ileoanal pouch for ulcerative colitis were studied. Eleven had pouchitis defined by the pouchitis disease activity index of > or =7 points and 7 had no history of pouchitis. Biopsies taken at the site of inflammation or in the normal mucosa were scored for the histologic lesions, the intensity of neutrophil infiltration, and the presence of crypt abscesses. Mucosal IL-8 and IL-10 mRNA were quantified by competitive polymerase chain reaction. RESULTS: IL-8, IL-10, and IL-10/IL-8 mRNA were similar in patients with or without pouchitis. IL-8 mRNA levels were significantly higher in patients with a histologic score >2 (p = 0.01) and in patients with crypt abscesses (p = 0.01). IL-10/IL-8 mRNA was significantly lower in patients having a histologic score >2 (p = 0.019), a neutrophil infiltration > or =10% (p = 0.013), and crypt abscesses (p = 0.01). CONCLUSION: Histologic lesions of pouchitis are associated with a mucosal imbalance between IL-8 and IL-10. IL-10 could be proposed as a new treatment for pouchitis.