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PubMed2005

Variation in antibacterial and anti-inflammatory activity of different growth forms of Malva parviflora and evidence for synergism of the anti-inflammatory compounds.

Malva parviflora leaves and roots were collected from five sites within the Qacha's Nek District in Lesotho. These plants had two distinct growth forms--upright and prostrate. Hexane, methanol and water extracts were made from the plant material and tested for antibacterial and anti-inflammatory activity using the disc diffusion and cyclooxygenase-1 (Cox-1) bioassays, respectively. Hexane, methanol and water extracts made from Malva parviflora with a prostrate growth form inhibited the growth of Gram-positive and Gram-negative bacteria, while extracts made from plants with an upright growth form inhibited the growth of Gram-positive bacteria only. Cox-1 anti-inflammatory activity of hexane, methanol and water extracts did not show any variation between the two growth forms. The hexane extracts of both the leaves and roots were the most inhibitory. The water extracts had the least inhibitory activity. Bioassay-guided fractionation of the root dichloromethane extract showed that Cox-1 anti-inflammatory activity was caused by at least two compounds that acted synergistically to produce the biological effect.

Anti-Bacterial Agents↗

PubMed2005

The rationale for nonsteroidal anti-inflammatory drug therapy for inflammatory myofibroblastic tumors: a Children's Oncology Group study.

BACKGROUND: Inflammatory myofibroblastic tumors (IMTs) are neoplasms that are highly vascularized, have an intermediate prognosis, and are associated with infiltration, obstruction, local recurrence, and rare metastasis. Resection of large IMTs can lead to substantial morbidity and even mortality. Anecdotal experience suggests that nonsteroidal anti-inflammatory drugs may eradicate large IMTs or shrink them to a more readily resectable size and configuration. To support the hypothesis that nonsteroidal anti-inflammatory drugs are antiangiogenic for IMTs by interfering with vascular endothelial growth factor (VEGF) signaling via cyclooxygenase 2 (COX-2) inhibition, IMT specimens were immunohistochemically examined for expression of COX-2 enzyme and VEGF. METHODS: The diagnosis of IMT was confirmed in all 18 cases comprising the study. Intensity of COX-2 and VEGF staining was graded, and staining uniformity was examined. ALK-1 protein expression, found in up to two thirds of IMTs, was also determined. RESULTS: COX-2 and VEGF expression were identified in all tissue examined, with staining intensity varying independently. ALK-1 protein expression was identified in 33% of specimens. Its presence was not related to the intensity of COX-2 or VEGF staining. CONCLUSIONS: Our data suggest that the mediators of angiogenesis, VEGF and COX-2, are present and may play an important role in the growth of IMTs.

Activin Receptors, Type II↗

PubMed2003

Mesenteric inflammatory veno-occlusive disorder: a rare entity mimicking inflammatory bowel disorder.

Mesenteric inflammatory veno-occlusive disorder (MIVOD) is a rare variety of inflammatory bowel disease. In addition to the case presentation, pathogenesis, and conflicting clinical, endoscopic, and computed tomography findings, we present for the first time the angiographic findings that would provide important clues to distinguish MIVOD from the chronic idiopathic variety of inflammatory bowel disease and confirm the diagnosis of MIVOD. Final diagnosis is made on full-thickness biopsy. Although medical treatment of MIVOD is unsuccessful, surgical resection of the involved segment results in resolution of symptoms.

Angiography↗

PubMed1984

Inhibition of PG production by MDL 035, a new non-steroidal non-acidic anti-inflammatory compound, in rat gastric mucosa and inflammatory exudate.

The effects of 3-(1-methylethyl)-2-(4-methoxyphenyl)-3H-naphth [1,2-d]imidazole, MDL 035, a new non-steroidal non-acidic anti-inflammatory compound, on the production of prostaglandin (PG) in rat gastric mucosa in vivo and in vitro and in inflammatory exudate in vivo were studied. MDL 035 reduced PGE2 and 6-keto-PGF1 alpha levels more effectively in inflamed tissue than in gastric mucosa when assayed in in vivo experiments, whereas indomethacin and other non-steroidal anti-inflammatory drugs (NSAIDS) are equally effective in both systems. MDL 035 is almost as active as indomethacin when incubated with gastric tissue in vitro. The better gastric tolerance of MDL 035 than of other NSAIDS is discussed in relation to these differences in in vivo and in vitro effects.

6-Ketoprostaglandin F1 alpha↗

PubMed1998

Differing profiles of prostaglandin formation inhibition between selective prostaglandin H synthase-2 inhibitors and conventional NSAIDs in inflammatory and non-inflammatory sites of the rat.

The present study examined the inhibitory profiles of NS-398 and nimesulide against prostaglandin (PG) formation in inflammatory and non-inflammatory sites, and compared them with those of aspirin and indomethacin. In vitro, indomethacin inhibited PGH synthase (PGHS)-1 and PGHS-2 almost equally, while NS-398 and nimesulide inhibited only PGHS-2. NS-398 (1, 10 mg/kg) and nimesulide (3 mg/kg) slowed the rate of plasma exudation and thus the exudate accumulation in rat carrageenin-induced pleurisy. Aspirin (30, 100 mg/kg) and indomethacin (10 mg/kg) also reduced this rate. NS-398 and nimesulide reduced the PGE2 more potently than TXB2 and 6-keto-PGF1 alpha in the exudate. However, aspirin and indomethacin did not exhibit this selectivity. The levels of PGE2 correlated significantly with the plasma exudation rate. Moreover, nimesulide (3 mg/kg) did not affect PGE2 formation in rat stomachs injected with 1 M NaCl solution, while indomethacin (10 mg/kg) reduced it. Thus, NS-398 and nimesulide exhibit different inhibitory profiles from aspirin and indomethacin against PG formation. These results suggest that PGE2 may be produced by PGHS-2 in the inflammatory site, and may play a more prominent role than PGI2 in plasma exudation.

6-Ketoprostaglandin F1 alpha↗

PubMed1997

Quantification of inflammatory mediators in stool samples of patients with inflammatory bowel disorders and controls.

Previous studies indicated that eosinophils and mast cells accumulate and become activated in inflammatory bowel disorders. The aim of the study was to examine the presence of eosinophil and mast cell mediators in human stool samples of patients with inflammatory bowel disorders. We measured eosinophil cationic protein (ECP), eosinophil protein X (EPX), methylhistamine, and alpha 1-antitrypsin in fecal samples of 136 patients (62 Crohn's disease, 24 ulcerative colitis, 15 intestinal food allergy, 35 other gastrointestinal diseases) and 8 healthy controls. We found strongly elevated levels of ECP (median: 29, range: 0.4-1783 ng/g feces) and EPX (803, 10-33,225 ng/g) in all patients groups compared to controls (ECP: 1.5, 0.5-55 ng/g; EPX: 235, 12-746 ng/g). Similar results, albeit less pronounced, were obtained for methylhistamine and alpha 1-antitrypsin. Particularly high concentrations of ECP and EPX were found in patients with active mucosal inflammation. In conclusion, the study presents an easy and reliable method for the detection of fecal ECP, EPX, and methylhistamine and may provide a tool to gain insight into the pathogenesis of inflammatory bowel diseases and have potential as diagnostic test.

Adolescent↗

PubMed2000

Filiform polyposis of the colon in chronic inflammatory bowel disease (so-called giant inflammatory polyps).

On the basis of 3 of our own cases, we describe unusually intense forms of filiform polyposis and local giant polyposis as a consequence of chronic inflammatory bowel disease. The patients are: A 52-year-old woman who for 7 years has been known to have Crohn's disease (CD); a 55-year-old man who for 14 years has been known to have chronic inflammatory bowel disease, which was first thought to have been ulcerative colitis, but, as a result of the findings on the subtotal colectomy specimen, had to be classified as Crohn's disease or colitis indeterminate; and a 53-year-old woman known to have had ulcerative colitis for 37 years. From the literature on the subject, we drew up a chronological list of a total of 43 cases with similar or completely identical findings. The clinical significance of the findings in their particularly massive intensity results from their necessary differentiation--in the context of differential diagnosis--from a malignant tumor, in particular from a carcinoma in association with chronic inflammatory bowel disease, or from a villous adenoma. The indication of a need to operate results from the impossibility of being able definitely to rule out a malignant degeneration by means of clinical methods. Also, experience shows that with massive findings of the kind described a spontaneous disappearance cannot be expected. Finally, too, the clinical symptoms and the patients subjective complaints necessitate balanced surgical treatment, taking into consideration the site and the extent of the lesion.

Colectomy↗

PubMed1999

Defining therapeutic targets by using adenovirus: blocking NF-kappaB inhibits both inflammatory and destructive mechanisms in rheumatoid synovium but spares anti-inflammatory mediators.

The role of the transcription factor NF-kappaB in the pathogenesis of rheumatoid arthritis has long been a subject of controversy. We used an adenoviral technique of blocking NF-kappaB through overexpression of the inhibitory subunit IkappaBalpha, which has the advantage that it can be used in the diseased tissue itself, with >90% of the synovial macrophages, fibroblasts, and T cells infected. We found that the spontaneous production of tumor necrosis factor alpha and other pro-inflammatory cytokines is NF-kappaB-dependent in rheumatoid synovial tissue, in contrast to the main anti-inflammatory mediators, like IL-10 and -11, and the IL-1 receptor antagonist. Of even more interest, IkappaBalpha overexpression inhibited the production of matrix metalloproteinases 1 and 3 while not affecting their tissue inhibitor. Blocking NF-kappaB in the rheumatoid joint thus has a very beneficial profile, reducing both the inflammatory response and the tissue destruction. The adenoviral technique described here has widespread applicability, allowing rapid testing of the effects of blocking a potential therapeutic target in either cultures of normal cells or in the diseased tissue itself.

Adenoviridae↗

PubMed2000

Anti-inflammatory response of IL-4, IL-10 and TGF-beta in patients with systemic inflammatory response syndrome.

The systemic inflammatory response syndrome (SIRS) is an inflammatory process seen in association with a large number of clinical infective and non-infective conditions. The aim of this study was to investigate the role of anti-inflammatory cytokines such as interleukin-4 (IL-4), interleukin-10 (IL-10), and transforming growth factor-beta (TGF-beta). Serum levels of IL-4, IL-10 and TGF-beta were determined in 45 patients with SIRS: 38 patients had SIRS of infectious origin, whereas seven patients had non-infectious SIRS. Twenty healthy subjects were used as controls. Serum levels of IL-4, IL-10 and TGF-beta were determined by an immunoenzyme assay. A significant increase of IL-4 was observed in these patients at the time of diagnosis and 5 days later. In contrast, serum levels of IL-10 were not increased at the time of diagnosis, but a slight decrease was noted after 5 days. Serum levels of TGF-beta were not increased at time of diagnosis, and a slight increase was observed after 5 days. Serum levels of IL-4 were significantly higher in patients with infectious SIRS at the time of diagnosis, whereas no significant difference between infectious and non-infectious SIRS was noted for serum levels of IL-10 and TGF-beta at the time of diagnosis and 5 days later. During SIRS, serum levels of IL-4 were significantly increased with a significant correlation between IL-4 and mortality, and only levels of IL-4 were significantly increased in the SIRS caused by infectious stimuli.

Adult↗

PubMed1993

Formation of eosinophilic and monocytic intradermal inflammatory sites in the dog by injection of human RANTES but not human monocyte chemoattractant protein 1, human macrophage inflammatory protein 1 alpha, or human interleukin 8.

Equilibrium binding studies on canine mononuclear and granulocytic cells allow the identification of a single high affinity receptor for the human C-C chemokine RANTES (dissociation constant, 14 +/- 8 pM), that, in contrast to the human RANTES receptor, has no affinity for human macrophage inflammatory protein 1 alpha (hMIP-1 alpha). A single intradermal injection of hRANTES in dog resulted in eosinophil- and macrophage-rich inflammatory sites within 4 h. Cell infiltration peaked at 16-24 h after hRANTES injection. There was histological evidence of intravascular activation of eosinophils at 4 h, although eosinophils in the vasculature and interstitium contained apparently intact granules. Monocytes were the predominant cells adherent to venular endothelium at 16-24 h. Human MIP-1 alpha elicited no response in canine dermis, whereas monocyte chemoattractant protein 1 caused mild perivascular cuffing with monocytes. In contrast, human interleukin 8 induced a neutrophilic dermal infiltrate that was maximal by 4 h after challenge. This provides the first direct evidence in vivo that RANTES has significant proinflammatory activity and, in addition, could be a mediator in atopic pathologies characterized by eosinophilic and monocytic inflammatory responses.

Animals↗

PubMed2000

Stimulation of macrophage inflammatory protein-1alpha, macrophage inflammatory protein-1beta, and RANTES by Candida albicans and Cryptococcus neoformans in peripheral blood mononuclear cells from persons with and without human immunodeficiency virus infection.

The beta-chemokine macrophage inflammatory protein (MIP)-1alpha, MIP-1beta, and RANTES are critical for recruitment of inflammatory cells into infected tissue. Moreover, by binding to the human immunodeficiency virus (HIV) coreceptor CCR5, release of these chemokines could influence the course of HIV infection. beta-chemokine gene expression and release was determined by ELISA and RNase protection assay, respectively, in peripheral blood mononuclear cells (PBMC) from HIV-negative and -positive persons stimulated with Candida albicans and Cryptococcus neoformans, 2 fungi common in HIV-infected persons. Gene expression and/or release of all 3 chemokines was seen in response to both fungi although C. albicans was more potent than C. neoformans. Fungal stimulated chemokine production by HIV-positive PBMC was similar to that in HIV-negative PBMC, suggesting that the scant inflammatory response often seen in AIDS patients with cryptococcosis and candidiasis is not secondary to suboptimal beta-chemokine release.

AIDS-Related Opportunistic Infections↗

PubMed1999

Development and subsequent refinement of the inflammatory bowel disease questionnaire: a quality-of-life instrument for adult patients with inflammatory bowel disease.

BACKGROUND: Health-related quality of life (HRQOL) describes the physical, social, and emotional attitudes and behavior of people in relation to health status. By the 1980s, HRQOL was noted to be impaired in chronic diseases but inflammatory bowel disease, had not been extensively described. METHODS: This review summarizes the results of several studies describing the development and application of a disease-specific HRQOL instrument, the Inflammatory Bowel Disease Questionnaire (IBDQ). RESULTS: An initial study described how patients with inflammatory bowel disease identified 150 problems they had experienced in four domains: bowel, systemic, emotional, and social function. Almost half of patients underreported impairment until encouraged by a reminder list. Thirty-two questions were included in the final questionnaire and were scored on a 7-point scale from I (worst) to 7 (best) for a range of possible scores from 32 to 224. Physicians' and spouses' global assessments correlated poorly with patient-reported HRQOL. Subsequent validation of the IBDQ suggested a strong correlation with disease severity (r = -0.5; p < 0.001) and a test-retest reliability of 0.7. Mean score changes of 16 to 30 points have been linked to changes in therapy. Statistically significant differences also occur between active and inactive disease. Results of four clinical trials have included the IBDQ as a measure of outcome. A self-administered version and a shortened version of the IBDQ have also been validated. CONCLUSIONS: The IBDQ is a valid, reliable, and sensitive measure that can be meaningfully applied in clinical trials. The short IBDQ may also be useful in clinical research and office practice.

Adult↗

PubMed1999

Advances in chronic inflammatory demyelinating polyneuropathy: disease variants and inflammatory response mediators and modifiers.

Available data on the immunopathogenesis of chronic inflammatory demyelinating polyneuropathy remain still fragmentary and insufficient for a unified hypothesis. Macrophage-mediated demyelination appears to play a fundamental role and cytokines, especially tumour necrosis factor-alpha, participate in this process. The nature of antigen presenting cells, T-cell receptors, adhesion molecules between inflammatory cells and myelinated fibers and the apparent predominance of T helper cell 1-related cytokines need to be explored to design more specific immunotherapies. In chronic cases of chronic inflammatory demyelinating polyneuropathy, a concomitant axonal loss secondary to primary demyelination is common and should be taken into consideration in the design of future therapeutic strategies.

Antigens, Viral↗

PubMed2003

An anti-inflammatory oligopeptide produced by Entamoeba histolytica down-regulates the expression of pro-inflammatory chemokines.

Axenically grown Entamoeba histolytica produces a pentapeptide (Met-Gln-Cys-Asn-Ser) with anti-inflammatory properties that, among others, inhibits the in vitro and in vivo locomotion of human monocytes, sparing polymorphonuclear leucocytes from this effect [hence the name originally given. Monocyte Locomotion Inhibitory Factor (MLIF)]. A synthetic construct of this peptide displays the same effects as the native material. We now added MLIF to resting and PMA-stimulated cells of a human monocyte cell line and measured the effect upon mRNA and protein expression of pro-inflammatory chemokines (RANTES, IP-10, MIP-1alpha, MIP-1beta, MCP-1, IL-8, I-309 and lymphotactin) and the shared CC receptor repertoire. The constitutive expression of these chemokines and the CC receptors was unaffected, whereas induced expression of MIP-1alpha, MIP-1beta, and I-309, and that of the CCR1 receptor--all involved in monocyte chemotaxis--was significantly inhibited by MLIF. This suggests that the inhibition of monocyte functions by MLIF may not only be exerted directly on these cells, but also--and perhaps foremost--through a conglomerate down-regulation of endogenous pro-inflammatory chemokines.

Animals↗

PubMed2005

Strong inflammatory cytokine response in male and strong anti-inflammatory response in female kidney transplant recipients with urinary tract infection.

Urinary tract infection (UTI) is the most common post-transplant infection in renal transplant recipients. The relationship of plasma and urine cytokines with UTI after kidney transplantation has not yet been delineated and literature reports on cytokine and UTI are rare. In a retrospective study, we compared post-transplant plasma and urine cytokine levels of 132 outpatient renal transplant recipients with or without UTI. Soluble interleukin-1 receptor antagonist (sIL-1RA), IL-2, sIL-2R, IL-3, IL-4, IL-6, sIL-6R, IL-8, IL-10, transforming growth factor-beta2 (TGF-beta2), interferon-gamma (IFN-gamma), and tumor necrosis factor-alpha (TNF-alpha) levels were determined using commercially available enzyme-linked immunosorbent assay (ELISA) kits. We found gender-related urine cytokine patterns. Anti-inflammatory sIL-1RA was significantly higher in females than in males and this gender-related difference was more pronounced in bacteriuric (P < 0.0001) than in nonbacteriuric (P = 0.001) patients. Urine proinflammatory cytokines IL-6 (P = 0.001) and IL-8 (P = 0.007) were significantly higher in male patients with bacteriuria than in males without bacteriuria and sIL-2R (P = 0.001) and sIL-6R (P = 0.03) were significantly higher in males with leukocyturia than in males without leukocyturia. Bacteriuria in males was associated with higher doses of immunosuppressive drugs (P = 0.02). Male renal transplant recipients with UTI have a strong inflammatory cytokine response with activation of IL-6, IL-8, sIL-2R and sIL-6R producing cells, whereas female patients with UTI block the inflammatory response to UTI by production of sIL-1RA.

Anti-Inflammatory Agents↗

PubMed2001

Effects of nonsteroidal anti-inflammatory drugs on Helicobacter pylori-infected gastric mucosae of mice: apoptosis, cell proliferation, and inflammatory activity.

Helicobacter pylori and nonsteroidal anti-inflammatory drugs (NSAIDs) are two well-known important causative factors of gastric damage. While H. pylori increases apoptosis and the proliferation of gastric epithelial cells and is an important factor in peptic ulcer and gastric cancer, NSAIDs induce cell apoptosis and have antineoplastic effects. We investigated the effects of NSAIDs (a nonselective cyclooxygenase [COX] inhibitor [indomethacin] and a selective COX-2 inhibitor [NS-398]) on the apoptosis and proliferation of gastric epithelial cells and gastric inflammation in H. pylori-infected mice. C57BL/6 mice were sacrificed 8 weeks after H. pylori SS1 inoculation. Indomethacin (2 mg/kg) or NS-398 (10 mg/kg) was administered subcutaneously once daily for 10 days before sacrifice. The following were assessed: gastric inflammatory activity, gastric COX protein expression by Western blotting; gastric prostaglandin E(2) levels by enzyme immunoassay, apoptosis by terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling, and cell proliferation by Ki67 immunostaining. Compared to the controls, H. pylori infection and/or NSAID treatment increased COX-1 and COX-2 protein expression. Gastric prostaglandin E(2) levels, apoptotic index, cell proliferation index, neutrophil activity, and the degree of chronic inflammation were all increased by H. pylori infection, and these effects were significantly decreased by indomethacin treatment. However, NS-398 treatment after H. pylori infection did not induce a significant reduction, although it did result in a tendency to decrease. These results show that NSAIDs can reverse the increased apoptosis and proliferation of epithelial cells and inflammatory activity in the stomachs of H. pylori-infected mice and that, like COX-2 activation, COX-1 induction contributes to the change of gastric mucosal cell turnover and inflammation induced by H. pylori infection.

Animals↗

PubMed2005

Systemic administration of the chemokine macrophage inflammatory protein 1alpha exacerbates inflammatory bowel disease in a mouse model.

INTRODUCTION: Exacerbations of inflammatory bowel disease are thought to be related to concurrent infections. As infections are associated with elevated local and serum concentrations of chemokines, we have determined whether systemic administration of the CC chemokine macrophage inflammatory protein 1alpha (MIP-1alpha) exacerbates colitis in a mouse model. METHODS: Colitis was induced in Balb/c mice using trinitrobenzene sulfonic acid (TNBS). Starting four days later, animals received daily intraperitoneal injections of recombinant MIP-1alpha. On day 7, mice were killed and pieces of colon taken for immunohistology and polymerase chain reaction analysis. The direct effects of MIP-1alpha on mucosal T cells and fibroblasts in vitro were also investigated. RESULTS: Systemic administration of MIP-1alpha markedly enhanced colitis with mice developing large transmural ulcers filled with granulation tissue. Treatment resulted in increased numbers of CD4 cells infiltrating the colonic lamina propria, increased interferon gamma (IFN-gamma) levels, and increased transcripts for tumour necrosis factor alpha (TNF-alpha) and matrix metalloproteinase 3 (MMP3). Isolated lamina propria lymphocytes from mice with TNBS colitis contained increased numbers of IFN-gamma and TNF-alpha transcripts when stimulated with MIP-1alpha in vitro. Colonic lamina propria fibroblasts also responded to MIP-1alpha with increased proliferation and decreased collagen 1 synthesis but fibroblast proliferation was not seen in vivo. CONCLUSIONS: These experiments show that increasing serum concentrations of a chemokine, MIP-1alpha, exacerbates immune mediated colitis. The effect seems to be due to the ability of MIP-1alpha to boost Th1 responses in the gut wall. Our findings also suggest a potential pathway by which peripheral infections can exacerbate inflammatory bowel disease.

Animals↗

PubMed2001

The immuno-inflammatory mechanism for tissue injury in inflammatory bowel disease and Helicobacter pylori-infected chronic active gastritis. Roles of the mucosal immune system.

The gastrointestinal mucosa is exposed to myriads of infectious and food antigens, and a unique barrier mechanism handles them on the mucosal surface, and specific immune responses to these antigens call on the mucosal immune system in the mucosal tissues to maintain homeostasis of gastrointestinal functions and structure. Abrogation of these mucosal defense mechanisms may lead to alter immunologic homeostasis in the gastrointestinal tract and to induce pathological features of inflammatory bowel disease (IBD) and Helicobacter pylori-infected chronic active gastritis, including chronic active inflammation, mucosal atrophy and tissue injuries. Regardless of the initiating cause of these long-standing chronic active mucosal inflammations, characteristic immuno-inflammatory mechanisms are involved in their pathogenesis, that is, similar and/or different specific prolonged impaired and excessive immuno-inflammatory responses following the abrogation of the mucosal barrier system are present in the diseased mucosa with IBD and H. pylori infection, respectively.

Apoptosis↗