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PubMed2005

Up-regulation of cyclooxygenase-2 by interleukin-1beta in colon carcinoma cells.

Growing evidence shows that Interleukin (IL)-1beta and Cyclooxygenase 2 (COX-2) play a crucial role in the pathogenesis of inflammatory diseases and tumor growth, particularly in the gastrointestinal tract. Here, we have analyzed the regulation of COX-2 by IL-1beta in the human colon carcinoma cell line Caco-2, showing that COX-2 induction by this cytokine is due to both nuclear factor (NF)-kappaB-dependent transcriptional and p38 mitogen-activated protein kinase (MAPK)-mediated post-transcriptional mechanisms. Treatment of these cells with IL-1beta increased the levels of COX-2 mRNA and protein and hence the production of PGE2. IL-1beta induced NF-kappaB activation in Caco-2 cells, promoting the binding of this transcription factor to DNA and increasing NF-kappaB-dependent transcription. Inhibition of NF-kappaB activation diminished IL-1beta-mediated transcriptional activation of COX-2. Furthermore, mutation or deletion of a putative NF-kappaB binding site in the human COX-2 promoter greatly diminished its induction by IL-1beta. In addition, this cytokine induced a rapid increase in p38 MAPK activation. Interestingly, inhibition of p38 MAPK by SB203580 severely decreased induction of COX-2 expression by IL-1beta. p38 MAPK signalling was required for IL-1beta-dependent stabilization of COX-2 transcript. Given the importance of COX-2 expression in intestinal inflammation and colon carcinogenesis, these findings contribute to determine the key signalling pathways involved in the regulation of COX-2 expression in colorectal cells by inflammatory stimuli, such as IL-1beta.

Caco-2 Cells↗
PubMed2006

Advances and perspectives in the genetics of inflammatory bowel diseases.

Several clinical and biological phenotypes define complex diseases such as inflammatory bowel disease (IBD). There is a critical role of the caspase recruitment domain protein 15/nucleotide-binding oligomerization protein 2-dependent (CARD15-NOD2) sensing of bacterial cell wall components in health and disease. The current etiologic model for IBD emphasizes an interaction between susceptibility and modifier genes along with environmental factors. Together, these lead to disease progression. However, further work should clarify the pathophysiological mechanisms leading to IBD and how innate immune signaling confers susceptibility to intestinal inflammation. This is a prerequisite for rational clinical management of IBD. Genetic, functional, serologic testing and development of therapeutics in IBD are discussed.

Crohn Disease↗
PubMed2004

Glutamine metabolism in Crohn's disease: a stable isotope study.

AIMS: To determine whether chronic intestinal inflammation alters glutamine utilization, six 31 +/- 6 yr-old patients with Crohn's disease and an age-matched group of 6 healthy subjects received 7-h intravenous infusions of L-[5,5,5-2H3]leucine, along with an infusion of L-[1-13C]glutamine delivered intravenously for the first 3.5 h, and via a nasogastric tube for the subsequent 3.5 hrs. None of the patients was receiving any nutritional supplement or antiinflammatory drug. All were in remission (Crohn's disease activity index < 150) and in a near-normal nutritional status. METHODS: We used plasma 2H3-alpha-ketoisocaproate to determine leucine appearance rate (Ra), and plasma 13C-glutamine and breath 13CO2 to determine glutamine Ra and oxidation, respectively. The fraction of enteral glutamine undergoing uptake in the splanchnic bed was determined from the difference in plasma 13C-glutamine enrichments between the intravenous and nasogastric 13C-glutamine infusion periods. RESULTS: Neither leucine Ra, nor plasma glutamine concentration (526 +/- 40 vs. 530 +/- 50 micromol/l), glutamine Ra (364 +/- 19 vs. 355 +/- 24 micromol kg(-1) h(-1)), or splanchnic glutamine uptake (61 +/- 5 vs. 65 +/- 2%) differed between groups. In both groups, glutamine oxidation rose when the glutamine tracer was supplied enterally, compared with the intravenous route (70 +/- 6 vs. 39 +/- 2% in patients; 69 +/- 2 vs. 38 +/- 1% in controls), but did not differ between groups. CONCLUSION: When in remission, patients with Crohn's disease have normal rates of proteolysis, and glutamine production, utilization, oxidation, and splanchnic uptake. The data suggest there is no obvious requirement for glutamine in patients with quiescent Crohn's disease.

Adult↗
PubMed2004

Protease-activated receptors: protease signaling in the gastrointestinal tract.

Serine proteases from the circulation, inflammatory cells, digestive glands and microorganisms can signal to cells by cleaving protease-activated receptors (PARs), a family of four G-protein-coupled receptors. Proteases cleave PARs at specific sites to expose tethered ligand domains that bind to and activate the cleaved receptors. Despite this irreversible mechanism of activation, PAR signaling is tightly regulated to prevent the uncontrolled stimulation of cells. Although PARs are found in all organ systems, protease signaling is of particular interest in the gastrointestinal tract, where proteases regulate neurotransmission, secretion, motility, epithelial permeability and intestinal inflammation, and can thus contribute to disease.

Animals↗
PubMed2004

Infliximab heals intestinal inflammatory lesions and restores growth in children with Crohn's disease.

BACKGROUND: Infliximab has recently emerged as an efficacious agent for patients with severe Crohn's disease. There are only few studies on the use of infliximab in children with Crohn's disease: most of them are retrospective and deal only with the clinical response to the drug. AIM: We aimed at assessing the efficacy of infliximab in children and adolescents with severe Crohn's disease recruited consecutively and followed up prospectively at a single centre. Clinical response, intestinal inflammation and growth pattern were evaluated. PATIENTS: Eighteen patients entered into the trial (median age: 13 years, range: 6-18). They were referred because of severe symptoms with unsatisfactory response to conventional drugs. METHODS: All patients received a baseline schedule of three intravenous infusions of infliximab (0, 2 and 6 weeks), 5 mg/kg. Paediatric Crohn's Disease Activity Index, nutritional and activity serum variables, and ileocolonoscopy (with histology) were evaluated before and 8 weeks after beginning the therapy. All patients had long-term administration of azathioprine (2 mg/kg per day). After the baseline schedule, eight patients had a retreatment infusion of infliximab (5 mg/kg) every 8 weeks. Weight and height Z scores were measured before starting the baseline infusion programme and after 6 months. RESULTS: After 8 weeks of therapy, there was a dramatic improvement in Paediatric Crohn's Disease Activity Index, in nutritional and activity blood parameters, as well as in endoscopic and histological scores; 10 patients had a clinical remission (Paediatric Crohn's Disease Activity Index < or = 10), 12 patients had an inflammatory remission (decrease in both endoscopic and histological scores for > or = 50% as compared to baseline values). In all patients corticosteroids were stopped within 4 weeks after beginning infliximab therapy. After 6 months of therapy, Paediatric Crohn's Disease Activity Index was markedly lower than the pre-treatment value; however, it was significantly lower in patients on retreatment than in those who received only three infusions of infliximab. Furthermore, a significant increase in both weight and height Z scores was observed 6 months after beginning of the baseline infusion programme. Moreover, weight and height gain was significantly higher in patients on retreatment rather than in those treated only with three baseline infusions of infliximab. Mild infusion reactions controlled by slowing infusion rate were observed in four patients. No delayed hypersensitivity-like reactions were seen. CONCLUSIONS: In children with severe Crohn's disease, infliximab is a safe and valuable treatment in inducing remission, in healing inflammatory lesions of the gut, as documented by endoscopy and histology, and in promoting growth. Retreatment infusions of infliximab may be suggested in childhood-onset Crohn's disease to maintain remission and reverse growth failure.

Adolescent↗
PubMed2005

Early or late guided missile in the treatment of Crohn's disease?

Over the last few years, much light has been shed on the pathogenesis of Crohn's disease. Further knowledge in this field has provided a firm basis not only in the understanding of current treatment but also for the development of new therapeutic strategies. Aim of these new agents is primarily to selectively interact with the key processes of intestinal inflammation. At present, only anti-tumour necrosis factor-alpha antibodies namely infliximab, is licensed for clinical practice but it is feasible to foresee that, in the near future, a larger range of these agents will become available. Herein, the most promising biological agents in the treatment of Crohn's disease are outlined, which patients would benefit from these agents and when they should be administered. Attention is focused on the early (top-down) or late (step-up) use of biological agents, which for their very targeted mechanism of action may be compared to guided missiles. As yet, early use of biological agents remains to be supported by convincing evidence, nevertheless it may be advocated as first-line therapy for newly diagnosed severe Crohn's disease patients, both adults and children.

Antibodies, Monoclonal↗
PubMed2005

Meprin metalloprotease expression and regulation in kidney, intestine, urinary tract infections and cancer.

Meprins are unique plasma membrane and secreted metalloproteinases that are highly regulated at the transcriptional and post-translational levels. Meprin alpha and beta subunits are abundantly expressed in kidney and intestinal epithelial cells, are secreted into the urinary tract and intestinal lumen, and are found in leukocytes and cancer cells under certain conditions. Their location and proteolytic activities indicate functions at the interface of the host and the external environment, and in trafficking of macrophages and metastases of cancer cells. These proteases can be detrimental when there is tissue damage or disruption, as in acute renal injury or intestinal inflammation, and there is evidence they are involved in movement of leukocytes and cancer cells to sites of infection or in metastasis, respectively.

Animals↗
PubMed2004

Treatment of inflammatory bowel disease with antibiotics.

Although antibiotics are clearly recognized as having a role in treating the infectious complications of inflammatory bowel diseases (IBD), their impact in the primary treatment of IBD has long been an area of speculation. Over the past decade there is increasing evidence that luminal gut bacteria play a role in the pathogenesis of IBD, particularly Crohn's disease. Compelling evidence that normal commensal bacteria induce chronic intestinal inflammation in susceptible rodents provides an excellent rationale for treatment of human IBD with antibiotics. This article summarizes published studies of antibiotics in IBD patients and reviews available data for the use of antibiotic therapy in Crohn's disease and ulcerative colitis.

Anti-Bacterial Agents↗
PubMed2006

Inflammatory bowel disease: current insights into pathogenesis and new therapeutic options; probiotics, prebiotics and synbiotics.

Inflammatory bowel disease (IBD) is a chronic relapsing disorder involving a dysregulated host-microbiota interaction. IBD patients have been shown to possess an increased risk for the development of colorectal cancer. Recently, focus has been placed on probiotic and prebiotic therapies, which aim to restore balance to the gastrointestinal microbiota, and reduce intestinal inflammation. Probiotics have been assessed extensively in animal models, with a number of clinical trials also demonstrating potential therapeutic benefits. However, it is widely accepted that more double-blind randomised placebo-controlled trials are required. Future research also needs to focus on determining which probiotics are the most efficacious in the IBD setting, and how the genetic and bacterial profiles of the patient will influence treatment responsiveness. Prebiotics have been studied less extensively, however, they may become an ideal treatment or co-treatment option due to their capacity to increase endogenous lactobacillus and bifidobacteria. Probiotics and prebiotics may offer a new therapeutic option for the treatment of IBD, however, a greater understanding of the mechanisms behind their action on the gastrointestinal microbiota is required in order to determine which probiotic, prebiotic or combinations thereof are the most beneficial.

Animals↗
PubMed2005

Administration of agonistic anti-4-1BB monoclonal antibody leads to the amelioration of inflammatory bowel disease.

4-1BB (CDw 137), a member of the tumor necrosis factor receptor (TNFR) superfamily, is a costimulatory receptor primarily expressed on activated T cells. It has been shown that the administration of agonistic anti-4-1BB monoclonal antibody (mAb) enhances tumor immunity and allogenic immune responses. Paradoxically, we found that the administration of anti-4-1BB mAb reduced the incidence and severity of inflammatory bowel disease. In this study, we investigated the effects of anti-4-1BB mAb in a murine intestinal inflammation model, which induced by the hapten reagent, 2,4,6-trinitrobenzene sulfonic acid (TNBS) and mimics immunologic characteristics of human Crohn's disease (CD). Colitis was induced by rectal administration of 2mg of TNBS in 35% ethanol using a vinyl catheter positioned 4cm from the anus. All mice were sacrificed 3 and 10 days after the TNBS administration. The disease activity index (DAI), histological changes of the colon and production of cytokines (IL-2, IL-4, IL-10 and IFN-gamma) were evaluated. The surface molecules of T cells in peripheral blood, spleen and mesenteric lymph nodes were analyzed by flow cytometry. When mice were treated with anti-4-1BB mAb, improvement in both wasting and histopathologic signs of colonic inflammation was observed. The increase a number of splenic CD4(+)CD25(+) T cells and decreased synthesis of the Th1 cytokine IL-2 also occurred. Interestingly, increased production of Th1 cytokine IFN-gamma and proportion of CD8(+) T cells were observed in mice treated with anti-4-1BB mAb in comparison to the colitic mice. These studies show, for the first time, that agonistic anti-4-1BB mAb can improve experimental colitis by reduction of IL-2 and augmentation of CD4(+)CD25(+) regulatory T cells. TNBS colitis is Th1-mediated and has similar histologic features and distribution of inflammation to CD. This study suggests that anti-4-1BB mAb therapy could be effective in the treatment of patients with CD.

4-1BB Ligand↗
PubMed2006

Role of toll-like receptors in spontaneous commensal-dependent colitis.

Inflammatory bowel disease (IBD) is thought to result from a dysregulated interaction between the host immune system and its commensal microflora. Heterogeneity of disease susceptibility in humans and rodents suggest that multiple mechanisms are responsible for the etiology of IBD. In particular, deficiencies in anti-inflammatory and immune-suppressive mechanisms play an important role in the development of IBD. However, it is unknown how the indigenous microflora stimulates the immune system and how this response is regulated. To address these questions, we investigated the role of Toll-like receptor (TLR) signaling in the development of spontaneous, commensal-dependent colitis in interleukin (IL)-2- and IL-10-deficient mice. We report that colitis was dependent on TLR signaling in Il10(-/-) mice. In contrast, Il2(-/-) mice developed intestinal inflammation in the absence of TLR signaling pathways. These results demonstrate a differential role of innate immune recognition by TLRs in the development of commensal-dependent colitis.

Adaptor Proteins, Signal Transducing↗
PubMed2004

Interleukin-22 activates STAT3 and induces IL-10 by colon epithelial cells.

Human interleukin-22 (IL-22), a cytokine with structural homology to IL-10, is produced by activated T cells. The IL-22 receptor complex consists of a ligand-binding chain, the IL-22R1 and a signal-transducing chain, the IL-10R2. The aim of this study is to identify potential target cells and associated biological activity of IL-22 by identifying cell types that specifically express high levels of IL-22R1 as the expression of IL-10R2 is ubiquitous. Expression of IL-22R1 mRNA, as analyzed by real time quantitative polymerase chain reaction (PCR), was observed in human tumor cell lines of stromal or epithelial origin derived from liver, pancreas, colon and lung tissue. Furthermore, we examined the ability of IL-22 to activate the JAK-Signal Transducer and Activator of Transcription (STAT) pathway in epithelial cells of the colon. IL-22 induced the phosphorylation of STAT1 and STAT3 in Colo205, a colon epithelial cell line. Consequently, IL-22 upregulated mRNA for Suppressor of Cytokine Signaling 3 (SOCS3), a STAT3-responsive gene. Further analyses, by real time quantitative PCR, on a panel of chemokines and immune function related genes revealed that IL-22 induced expression of the acute phase proteins alpha-Antichymotrypsin and Serum Amyloid A, as well as IL-10 mRNA and protein production by Colo205. Induction of IL-10 by IL-22, in Colo205 cells, could be inhibited in the presence of a neutralizing antibody against IL-10R2. IL-22-mediated effects on the Colo205 cells were also inhibited in the presence of IL-22 binding protein (IL-22BP), a soluble receptor with structural similarity to IL-22R1. The high levels of expression of IL-22R1 observed in epithelial cells of the colon and the ability of IL-22 to upregulate production of acute phase proteins and IL-10 in Colo205 cells, suggest a functional role for IL-22 in intestinal inflammation.

Animals↗
PubMed2005

Development and validation of a novel IL-10 deficient cell transfer model for colitis.

A number of rodent models for inflammatory bowel disease (IBD) have been developed, but most cannot be used to develop and validate new therapies for IBD. From the models developed, the IL-10 deficient mouse model is the one that results in a disease similar to human IBD; however, in this model, colitis occurs with variable incidence taking 3-4 months to develop. These are serious problems with the model when evaluating a new therapy because of the large-scale experiments required and the difficulty in performing an accurate pharmacological analysis. In this study, the IL-10 deficient mouse model was modified by transferring whole spleen and mesenteric lymph node cells from IL-10 deficient mice to CB-17 SCID mice. In this IL-10 deficient cell transfer model, chronic intestinal inflammation developed in all recipients within 2-3 weeks, which was far earlier than in donor IL-10 deficient mice. The pathological phenotypes were similar to those of IL-10 deficient mice and CD45RBhi T cell-transfer models. In addition, we assessed several agents for inflammatory bowel disease to validate the general utility of this cell transfer model. It is worth noting that TNFR-Ig or prednisolone, which is effective for treatment of patients with severe-fulminant Crohn's disease, markedly attenuated pathological clinical indices in this colitis model, whereas the immunosuppressive agents, azathioprine, tacrolimus, and cyclosporine A produced no significant effect. These results suggest that the IL-10 deficient cell transfer model is a good experimental model to use for developing new and effective therapies for active IBD.

Adrenal Cortex Hormones↗
PubMed2006

Prevalence of Campylobacter species, Helicobacter pylori and Arcobacter species in stool samples from the Venda region, Limpopo, South Africa: studies using molecular diagnostic methods.

OBJECTIVES: This study determined the prevalence of Campylobacter spp., Helicobacter pylori and Arcobacter spp. in stool samples from Venda in relation to diarrhea, intestinal inflammation and HIV status using specific molecular methods. METHODS: Stool samples were collected from hospital patients (255) and primary school children (67). Genomic DNA was extracted from the stools and molecular methods including PCR, PCR followed by restriction analysis and multiplex PCR were used to test for the different organisms. The lactoferrin content of the stools was determined using commercial kits from TechLab (Blacksburg, VA, USA). RESULTS: The prevalence of the different organisms was 50.6% for H. pylori, 10.2% for C. jejuni, 6.2% for A. butzleri, 6.5% for C. coli, 3.1% for C. concisus, 2.8% for A. cryaerophilus and 1.9% for A. skirrowii. Of all the organisms, only C. jejuni was significantly associated with diarrhea (84.8%) (chi2=21.025, P<0.001) and elevated levels of lactoferrin (78.8%) (chi2=16.919, P<0.005) and was an important pathogen associated with diarrhea among HIV positive individuals (22.8%). CONCLUSIONS: Campylobacter infections are common causes of gastroenteritis in Venda. Non-C. jejuni/coli Campylobacters such as C. concisus as well as A. butzleri and H. pylori may be involved in gastrointestinal diseases in the region but further studies are needed to confirm this hypothesis.

Adolescent↗
PubMed2005

Acute ileal inflammatory cytokine response induced by irradiation is modulated by subdiaphragmatic vagotomy.

Neural involvement plays a role in the genesis of the peripheral inflammatory process that contributes to the irradiation intestinal disorders. However, little is known about the role of vagus nerve in modulating inflammatory process in rat. Here, we have shown that the NF-kappaB activation was consistent with the acute overexpression of pro-inflammatory cytokines (IL- 1beta, TNF-alpha, IL-6) at 3, 6, and 12 h induced by whole-body irradiation (8 Gy). Subdiaphragmatic vagotomy reduced NF-kappaB activation and cytokine transcription in the early period post-irradiation. In contrast, vagotomy amplified overexpression of irradiation-induced anti-cytokines (IL-10, IL-1Ra) and of receptors involved in anti-inflammatory effects (IL- 1RII, TNFRII). These results show that the vagus nerve is a pro-inflammatory pathway in early irradiation-induced intestinal inflammation.

Animals↗
PubMed2005

Antioxidants as novel therapy in a murine model of colitis.

Reactive oxygen species (ROS) are increased in inflammatory bowel disease (IBD) and have been implicated as mediators of intestinal inflammation. We investigated the hypothesis that antioxidants with diverse properties attenuate disease progression in a murine dextran sodium sulfate (DSS)-induced colitis model. These antioxidants were (A) S-adenosylmethionine, a glutathione (GSH) precursor; (B) green tea polyphenols, a well-known antioxidant; and (C) 2(R,S)-n-propylthiazolidine-4(R)-carboxylic acid (PTCA), a cysteine prodrug, involved in GSH biosynthesis. BALB/c mice were divided into four groups and provided with the above mentioned antioxidants or the vehicle incorporated into chow. The animals were further divided into two subgroups and given normal drinking water (control) or water supplemented with DSS (to induce colitis), and the progression of the disease was studied. DSS-treated mice developed severe colitis as shown by bloody diarrhea, weight loss and pathological involvement (P<.001). However, all the antioxidants significantly improved diarrhea and colon lesions (P<.01), and increased body weights (P<.05). Hematocrits were significantly less affected in DSS-treated animals receiving antioxidants (P<.01). Colon lengths were significantly decreased due to mucosal inflammation in DSS-treated animals, but antioxidant therapy normalized this pathological finding (P<.001). The blood level of reduced GSH was decreased in DSS-treated mice (P<.05) and returned to normal when treated with antioxidants. Serum amyloid A (acute phase protein; P=.0015) and tumor necrosis factor-alpha (TNF-alpha; pro-inflammatory cytokine; P<.01) were significantly increased in DSS-treated animals (161+/-40 pg/ml) and improved with antioxidant treatment (P<.01). Finally, actin cytoskeleton was distorted and fragmented in the mucosa of DSS-treated mice and improved with antioxidant therapy. In conclusion, three structurally dissimilar antioxidants provided protection against DSS-induced colitis in this murine model, supporting a possible role for antioxidant therapy in IBD patients.

Animals↗
PubMed2006

The Vitamin D analogue TX 527 blocks NF-kappaB activation in peripheral blood mononuclear cells of patients with Crohn's disease.

Crohn's disease (CD) is an inflammatory disease characterized by the activation of the immune system in the gut. Since tumor necrosis factor (TNF-alpha) plays an important role in the initiation and perpetuation of intestinal inflammation in CD, we investigated whether TX 527 [19-nor-14,20-bisepi-23-yne-1,25(OH)(2)D(3)], a Vitamin D analogue, could affect peripheral blood mononuclear cells (PBMC) proliferation and exert an immunosuppressive effect on TNF-alpha production in CD patients, and whether this immunosuppressive action could be mediated by NF-kappaB down-regulation. TX 527 significantly decreased cell proliferation and TNF-alpha levels. On activation, NF-kappaB, rapidly released from its cytoplasmatic inhibitor (IKB-alpha), transmigrates into the nucleus and binds to DNA response elements in gene promoter regions. The activation of NF-kappaB, stimulated by TNF-alpha, and its nuclear translocation together with the degradation of IKB-alpha were blocked by TX 527. At the same time, NF-kappaB protein levels present in cytoplasmic extracts decreased in the presence of TNF-alpha and increased when PBMC were incubated with TX 527. The results of our studies indicate that TX 527 inhibits TNF-alpha mediated effects on PBMC and the activation of NF-kappaB and that its action is mediated by Vitamin D receptor (VDR), which is activated when the cells are stimulated with TX 527.

Adult↗
PubMed2005

Bromelain improves decrease in defecation in postoperative rats: modulation of colonic gene expression of inducible nitric oxide synthase.

Ileus continues to be a common consequence of abdominal surgery, causing significant patient discomfort and often leading to more serious problems. The therapy available is limited, hence, ileus remains an important clinical problem. Activation of inducible nitric oxide synthase (iNOS) directly modulates intestinal dysmotility after bowel manipulation and plays an essential role in initiating intestinal inflammation. Nuclear factor (NF)-kappaB is known to be a critical component of iNOS gene transcriptional activation in response to inflammatory stimuli. Bromelain is a crude extract from the pineapple stem, which is sold as a nutritional supplement to "promote digestive health" and as an anti-inflammatory medication in some developed countries. Here, we have found that oral administration of bromelain improves decrease in defecation in abdominal postoperative rats. Results showed that bromelain increased the wet weight, dry weight, water content and number of fecal pellets in laparotomized plus mechanically manipulated rats, suggesting improvement of postoperative ileus. Furthermore, bromelain treatment inhibited overexpressed iNOS mRNA and restored down-regulated inhibitor kappaBalpha mRNA in the colon of the postoperative rats. From the in vitro experiments, bromelain inhibits lipopolysaccharide (LPS)-induced nitrite overproduction in macrophage cell lines and LPS-induced NF-kappaB luciferase reporter gene expression in RAW264.7 macrophages transfected with NF-kappaB luciferase reporter gene. Thus, our findings suggest that bromelain improves decrease in defecation in postoperative rats, at least in part, by inhibiting colonic iNOS overexpression via NF-kappaB pathway. Our data indicates that bromelain may benefit patients with postoperative ileus.

Animals↗