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PubMed2026

Stromal ARHGEF15 Correlates With Inflammatory EMT and Stromal-Immune Crosstalk During Inflammatory Bowel Disease-To-Colorectal Cancer Progression.

Patients with inflammatory bowel disease (IBD) have an increased risk of colorectal cancer (CRC), but how chronic intestinal inflammation drives malignant transformation remains unclear. We retrospectively reanalyzed published single-cell transcriptomic datasets from intestinal biopsies of healthy individuals and patients with IBD; differential expression was assessed using independent t tests with Benjamini-Hochberg false discovery rate correction. We then integrated those single-cell findings with the Cancer Genome Atlas bulk transcriptomes and pharmacogenomic cohorts to trace stromal programs across the IBD-to-cancer continuum. ARHGEF15 emerged as a stromal gene enriched in CD74hi HLA-DRB1hi arterial pericytes within inflamed tissue. Its expression rose steadily from IBD to CRC and tracked with epithelial-mesenchymal transition (EMT) activity. In CRC, higher ARHGEF15 expression was associated with shorter overall and progression-free survival. These retrospective, in silico findings identify ARHGEF15 as an exploratory stromal biomarker associated with inflammatory EMT and stromal-immune remodeling during IBD-to-CRC progression. Prospective experimental and clinical validation is required to establish its prognostic or therapeutic relevance.

ARHGEF15↗

PubMed2006

CCL2 as a trigger of manifestations of compensatory anti-inflammatory response syndrome in mice with severe systemic inflammatory response syndrome.

Patients with compensatory anti-inflammatory response syndrome (CARS) are at a higher risk for infection with various opportunistic pathogens. CARS develops commonly in association with the manifestation of systemic inflammatory response syndrome (SIRS). In the present study, the role of SIRS-associated soluble factors on the CARS development was examined in mice with pancreatitis, a carrier of typical SIRS. Following the production of SIRS-related cytokines [tumor necrosis factor alpha and interleukin (IL)-1beta], CC chemokine ligand 2 (CCL2), IL-4, and IL-10 (typical CARS cytokines) were detected in the sera of mice with pancreatitis. CCL2 has been described as an essential chemokine for the T helper cell type 2 manifestation. CARS effector cells (cells with an ability to produce IL-4 and IL-10) were not generated from normal T cells after stimulation with SIRS-related cytokines. However, these cells were generated from normal T cells after cultivation with peripheral blood neutrophils (PMN) from SIRS mice in a dual-chamber transwell. Normal T cells did not convert to CARS effector cells after transwell cultures with PMN from normal mice. CCL2 was detected in culture fluids of PMN from SIRS mice, and PMN from normal mice did not produce CCL2 into their culture fluids. CARS effector cells did not appear in PMN-depleted SIRS mice or SIRS mice treated with anti-CCL2 monoclonal antibody, and these cells were demonstrated in PMN-depleted SIRS mice after treatment with recombinant murine CCL2. These results indicate that CCL2 produced by PMN from SIRS mice is an active molecule on the SIRS-associated CARS manifestation.

Animals↗

PubMed1986

[Pharmacological studies on proglumetacin maleate, a new non-steroidal anti-inflammatory drug. (1). Anti-inflammatory effects].

Anti-inflammatory effects of proglumetacin maleate (PGM), a new indomethacin (IND) derivative, were compared with those of IND on an equimolar-dose basis. PGM produced a dose-dependent inhibition of vascular permeability and carrageenin edema. These inhibitory effects of PGM were greater when given 4 hr prior to phlogistic agents than when given 1 hr before. Moreover, these effects of PGM were long-acting. Inhibitory effects of PGM on kaolin edema and UV-erythema were slightly less active than those of IND. PGM markedly reduced the leukocyte migration in carrageenin pleurisy. Subacute anti-exudative and anti-granuloma effects of PGM were nearly equal to those of IND. Also, PGM showed strong prophylactic and therapeutic effects on adjuvant arthritis, the model of chronic (immuno-reactive) inflammation. These effects of PGM were superior or equal to those of IND. These pharmacological properties of PGM suggested its potential usefulness in rheumatic and other inflammatory disorders. It was considered that the mode of action of PGM mainly depended on its active metabolite, IND. However, PGM was also active in the case of local administration into the sites of inflammation on rat hind paw edema. Therefore, it seemed that PGM had a different behavior than a so called "prodrug".

Animals↗

PubMed1988

[A correlation between the species differences in anti-inflammatory activity of AD-1590, a non-steroidal anti-inflammatory drug, and its plasma level].

Authors have reported that the oral potency ratio of AD-1590 to indomethacin varies with the animal models employed; the ratio is 4, 2.3 and 31 in the tests of acetic acid-induced vascular permeability (male mice), carrageenan hind paw edema (male rats) and UV-erythema (female guinea pigs), respectively. Thus, the relationship between the difference in the anti-inflammatory activity of AD-1590 among animal models and the species difference of the plasma AD-1590 level was investigated in experimental animals in order to ascertain the cause of the difference in the potency ratio. Inhibitory potency of AD-1590 on UV-erythema and increased vascular permeability induced by acetic acid in male rats was about 2.1 and 2.3 times, respectively, that of indomethacin. On the other hand, after a single oral administration of 5 mg/kg, the highest plasma AD-1590 level was seen in female guinea pigs (AUC9-8 hr = 63.1 micrograms.hr/ml); and followed by that in mice (male, 32.1; female, 36.1) greater than male dogs (11.5) greater than or equal to rats (male, 9.02; female, 12.5), male rabbits (9.17) greater than male monkeys (9.34 at 6 mg/kg). Hucker et al. have reported that the plasma level of indomethacin in rats is several times higher than that in guinea pigs, rabbits and monkeys. These results suggest that most of the species difference in the relative potency of AD-1590 to indomethacin in the anti-inflammatory activity results from the species difference in the plasma level of both drugs.

Animals↗

PubMed1994

The spinal actions of nonsteroidal anti-inflammatory drugs and the dissociation between their anti-inflammatory and analgesic effects.

The traditional classification of nonsteroidal anti-inflammatory drugs (NSAIDs) as exclusively 'peripherally acting' agents is no longer valid. For many of these agents there is a growing body of evidence in favour of an additional central mechanism for their anti-inflammatory and analgesic effects. This view is further supported by the recent discovery that a substantial component of the hyperalgesia and allodynia that characterise postinjury hypersensitivity occurs in the CNS, notably the spinal dorsal horn. An important corollary is that inhibition of central nociceptive processing may represent an important analgesic mode of action for those NSAIDs that are effective in the management of pain after tissue injury. Historically, attempts to group this heterogeneous class of compounds into a single entity are largely derived from the observation that the majority of clinically useful NSAIDs are weak organic acids (pKa 3 to 5), bind extensively to plasma albumin (= 99%), and inhibit (to varying degrees) prostaglandin synthesis. However, the significance of these various unifying features is becoming increasingly obscure. While inhibition of prostaglandin synthesis apparently remains an important analgesic mode of action for NSAIDs both in the periphery and the CNS, other mechanisms should be considered. Some NSAIDs, in addition to their effects on prostaglandin synthesis, also affect the synthesis and activity of other neuroactive substances believed to have key roles in processing nociceptive input within the dorsal horn. It has been argued that these other actions, in conjunction with inhibition of prostaglandin synthesis, may synergistically augment the effects of NSAIDs on spinal nociceptive processing. Despite much effort, it remains a formidable task to assess the significance of these differential mechanisms upon clinical pain states. In the meantime, however, it may be possible, on the basis of in vivo studies, to evaluate the impact of putative spinal analgesic mechanisms that are unrelated to inhibition of prostaglandin synthesis. This approach has recently been extended to include the identification of pharmacokinetic and clinical correlates of these derived in vivo parameters, and in this way attempt to demonstrate clinical relevance.

Analgesics↗

PubMedDate not supplied

[The prevalence of radiographic sacroiliitis in patients affected by inflammatory bowel disease with inflammatory low back pain].

Inflammatory bowel diseases (IBD), as Crohn's disease (CD) or ulcerative colitis (UC), are frequently complicated by joint complaints with prevalence that varies between 10 and 28%. The IBD related arthropathy may be expressed as peripheral arthritis or axial one frequently indistinguishable from the classical ankylosing spondylitis (AS). According to ESSG criteria for spondyloarthropathy, the presence of synovitis or the inflammatory back pain (IBP) in IBD patients is diagnostic for spondyloarthropathy, but for diagnosis of ankylosing spondylitis also radiological criteria must be fulfilled. There are few studies regarding the radiological prevalence of sacroiliitis in patients with IBD. We examined, by plain film radiograms of pelvis, 100 sacroiliac joints (SJ) of 50 IBD patients with IBP. The New York (1984) SJ radiological score with gradation from 0 to 4 was applied. Total sacroiliac score (SJS) was summarized between left and right side (from 0 to 8). Fourteen patients fulfilled New York modified criteria for AS and 8 patients had unilateral 2nd grade sacroiliitis. Only 4 of 14 AS patients (28%) were HLA B27 positive. Thirty patients had localized IBP, 10 extended to buttock and 4 extended to sacrum. Sixteen patients had sciatica-like extension of back pain. A difference in SJS between left and right side was observed only in CD patients (1.3 +/- 0.8 and 0.8 +/- 0.9 respectively; p < 0.05), but not in UC (1.5 +/- 1.2 vs 1.5 +/- 1.3; p = ns) nor in total IBD patients (1.4 +/- 1.0 vs 1.2 +/- 1.2; p = ns). Total SJS was higher in UC respect CD, but not significantly (2.9 +/- 2.3 vs 2.1 +/- 1.5; p = ns). Our data confirm the importance of these symptoms in patients with IBD, who need to be carefully investigated also for these aspects.

Adult↗

PubMed1979

Action of gold salts on the inflammatory response and inflammatory cell function.

Information relating to the effect and mechanism of action of gold salts on acute and chronic inflammatory processes has been reviewed. Gold salts are effective in suppressing various aspects of the acute inflammatory process although large gaps exist in the knowledge of the mechanisms involved. Available evidence indicates that gold salts affect many biochemical pathways and that interaction with enzymes plays a major role in their pharmacology. Because they are more difficult to investigate, the action of gold salts on various important aspects of chronic inflammation have not yet received much attention.

Animals↗

PubMedDate not supplied

Exploring the relationships between inflammatory response and coagulation cascade in inflammatory bowel disease.

BACKGROUND: The inflammatory network and the coagulation cascade are strictly correlated biological systems. Inflammatory Bowel Diseases (IBD) are characterised by a prothrombotic state, a hypercoagulability state and an increased prevalence of thromboembolic events. METHODS: We reviewed the IBD literature in which the relationships between inflammation and coagulation were evaluated. RESULTS: Several risk factors and mechanisms have been suggested to be implicated in determining the increased risk for thrombosis of IBD. Even if IBD may be per se a prothrombotic condition, systemic inflammation and vitamin deficiencies appear to play a relevant role in determining such a risk. CONCLUSIONS: A good and continuous control of the intestinal disease and vitamin supplementation are strongly recommended in order to correct some of the risk factors for thrombosis in IBD patients.

Blood Coagulation↗

PubMed1979

Comparison of the effects of a non-steroidal anti-inflammatory agent, an immunosuppressive, a corticosteroid and an immunomodulator on various immunological and non-immunological inflammatory experimental models.

The effects of a non-steroidal anti-inflammatory agent, phenylbutazone, a corticosteroid, desonide, an immunosuppressive, cyclophosphamide and an immunomodulator, levamisole on a number of experimental inflammatory models were compared. Compounds were first tested in carrageenin-induced pleurisy as a non-immune acute inflammation, then in passive skin anaphylaxis and reversed passive Arthus oedema in the rat as models of humoral immunity. Finally the compounds were investigated in various delayed hypersensitivity tests: reaction to sheep red cells and to oxazolone in the mouse, skin reaction to purified protein derivative (P.P.D.) in the rat and guinea-pig, P.P.D. induced pleurisy in the guinea-pig.

Animals↗

PubMed2006

Anti-inflammatory effects of insulin and pro-inflammatory effects of glucose: relevance to the management of acute myocardial infarction and other acute coronary syndromes.

Hyperglycemia worsens morbidity and mortality for patients in intensive care or with acute myocardial infarction, stroke, or coronary artery bypass grafts. The control of hyperglycemia with insulin improves clinical outcomes for patients with these conditions. This article reviews the anti-inflammatory effects of insulin and pro-inflammatory effects of glucose and free fatty acids, and provides a mechanistic justification for maintaining euglycemia with insulin infusions. Hyperglycemia induced by infusions of a fixed dose of insulin with high rates of glucose may neutralize the benefit of insulin, and such regimens should be replaced by infusion of insulin to restore and maintain euglycemia.

Acute Coronary Syndrome↗

PubMed1982

[Prostaglandins, leukotrienes, anti-inflammatory substances and their importance in inflammatory reactions of the skin].

Prostaglandins appear to play an important role as mediators of inflammation since they fulfill the major criteria. They possess powerful proinflammatory properties; they are present in increased concentrations in a wide range of proinflammatory lesions, and anti-inflammatory drugs inhibit their formation. The role of leukotrienes and other hydroxy fatty acid products is far less clear although their participation in cellular events seems probable. Steroid and nonsteroid anti-inflammatory drugs owe their activity at least in part to inhibition of biosynthesis of prostaglandins, although these two drug classes appear to act at different points in the pathways. It becomes increasingly clear that the oxygenation of arachidonic acid leads to the formation of a multiplicity of pharmacologically active fatty acids of which only a few have so far been identified.

Animals↗

PubMed1982

[Anti-inflammatory activity of a non-steroidal anti-inflammatory agent, zomepirac sodium, in experimental animals].

Anti-inflammatory and gastrointestinal ulcerogenic activities of zomepirac sodium were investigated in experimental animals. The inhibitory activity of zomepirac sodium against carrageenin hind paw edema in rats, acetic acid-induced increase in vascular permeability in mice, and UV-erythema in guinea pigs was more potent than that of indomethacin. Anti-edema activity of zomepirac sodium was seen in adrenalectomized rats. Zomepirac sodium, like indomethacin, inhibited the delayed phase of hind paw edema produced by mixed phlogistics, but not the early phase mediated by histamine and serotonin in rats. Zomepirac sodium produced a dose-dependent inhibition against granuloma formation, established adjuvant arthritis, and development of adjuvant arthritis in rats; and its activity was slightly less potent than that of indomethacin. The inhibitory activity of zomepirac sodium on PGE2 biosynthesis in vitro was about one-third that of indomethacin. The ulcerogenic activity of zomepirac sodium was about 5 times weaker than that of indomethacin. From these results, it was suggested that zomepirac sodium was effective on various types of inflammation and showed particularly potent inhibitory activity against acute inflammation. These findings suggest that the mode of action of zomepirac sodium is similar to that of other acidic non-steroidal anti-inflammatory drugs.

Adrenalectomy↗

PubMed1982

[Anti-inflammatory and analgesic activities of a trans-cutaneous non-steroidal anti-inflammatory agent, etofenamate gel].

Anti-inflammatory and analgesic activities of topically applied etofenamate gel (5% etofenamate) were investigated in experimental animals. Etofenamate gel showed a dose related inhibition against vascular permeability caused by histamine in mice and ultra violet light-induced erythema in guinea pigs at doses of 10--100 mg/site and 25--200 (ED50 = 26.6) mg/site, respectively. The erythema was not inhibited with its topical application of 100 mg/site to the skin distant from the erythema. Granuloma formation, caused by felt-pellet implantation, was inhibited in a dose dependent manner by repeated application of etofenamate gel (10--100 mg/site/day). Etofenamate gel inhibited the pain-like responses in both the arthritic joint and the edematous hind paw of rats with 50--200 mg/joint and 100 mg/paw, respectively. In these tests, the vehicle gel did not show any significant activity. The potency of etofenamate gel was stronger than that of adrenal-extracts ointment (Mobilat) and approximately comparable to indomethacin ointment (1% indomethacin) in a weight basis of formulations. Topical application of etofenamate (0.5--2 mg/ear) resulted in a dose related decrease of contact hypersensitivity to oxazolone in mice, and its activity was nearly equipotent to flufenamic acid and about one-fourth that of indomethacin. From these results, it was suggested that etofenamate gel, applied topically to the inflamed tissue, showed a certain inhibitory activity against acute and subacute-chronic inflammation and inflammatory pain-like responses.

Administration, Topical↗

PubMed1993

Investigations on the role of inflammatory and anti-inflammatory agents on the treatment of murine B cell leukemia by recombinant human interleukin-2.

Human recombinant interleukin-2 (rIL-2) was used in an effort to find effective biological therapy against the murine B-cell leukemia (BCL1), a spontaneous, nonimmunogenic, highly lethal leukemia of Balb/c origin. High dose rIL-2 (10(5) Cetus units 3 times a day for 5 days) was proven to be curative for mice inoculated with up to 10(4) BCL1 cells. Considering the fact that mice which showed more clinical signs of rIL-2 related toxicity had higher leukemia-free survival, and in view of the fact that BCL1 is a totally nonimmunogenic tumor, we have investigated the possible role of nonspecific effects of inflammatory and anti-inflammatory agents in order to speculate on the possible therapeutic role of inflammation on the overall effect of rIL-2 in the treatment of BCL1. According to the results presented in this work, it appears that although mediators of inflammation may play some role against leukemia, their overall effect in comparison with high-dose rIL-2 is relatively insignificant.

Animals↗

PubMed1995

[Effect of non-steroidal anti-inflammatory drugs on inflammatory reaction. An animal experiment study].

Previous investigations indicate that the application of a cyclooxygenase inhibitor alone can lead to amplification of the inflammatory process. To prevent this response a combination of flurbiprofen and leukotriene receptor antagonist (S 872419 A, Hoechst AG, Frankfurt/Main) were tested in an animal model. The right eye of 48 rabbits was burned with alcali (0.25 mol/l sodium hydroxide). Thirty animals were treated with (0.03% flurbiprofen sodium eye drops and 1% S872419 A eye drops, five times daily). Eighteen animals received no therapy for up to 14 days. Hyperemia of the limbal vessels, corneal vascularization, the number of PMNLs in the cornea and the prostacyclin level in the anterior chamber of the eye (ELISA) served as criteria. On day 3, after the chemical burn only the therapy group showed a significant decrease in hyperemia of the limbal vessels (14th day: score with therapy 0.3, without 2.17, P < 0.05). Without therapy corneal vascularization filled a much larger area from the 6th day on (14th day: area with therapy 3.5 mm2, without 63.7 mm2, P < 0.05). The number of PMNLs was effectively limited by therapy in the superficial stromal layers of the cornea and with therapy showed 2.4 cells/0.014 mm2 and without 18 cells/0.014 mm2 after 48 h. Without Therapy the level of prostacyclin was up to 15 times higher than with (12-h value with therapy) 607 pg/ml, without 9094 pg/ml, P < 0.05). Suppression of cyclo- and lipoxygenase-mediated inflammatory responses is possible with the combination of flurbiprofen and S 872419 A when two arachidonic by inhibition of prostanoid synthesis and leukotriene receptor block at the same time.

Animals↗

PubMed2000

Chronic infantile neurological cutaneous and articular/neonatal onset multisystem inflammatory disease syndrome: ocular manifestations in a recently recognized chronic inflammatory disease of childhood.

OBJECTIVE: To report on the ocular manifestations of the Chronic Infantile Neurological Cutaneous and Articular/Neonatal Onset Multisystem Inflammatory Disease (CINCA/NOMID) syndrome, a rare, recently identified, pediatric multisystem inflammatory disease with chronic cutaneous, neurological, and articular manifestations. DESIGN: Descriptive case-report study. SETTING: International collaborative study based on a questionnaire. RESULTS: We included 31 patients. The mean age at onset of eye manifestations was 4.5 years. Optic disc changes were the most common feature, occurring in 26 patients (83%), including optic disc edema, pseudopapilledema, and optic atrophy. Anterior segment manifestations varying from mild to severe were seen in 13 patients (42%); chronic anterior uveitis, in 17 patients (55%). Moderate to severe visual acuity loss in at least 1 eye was seen in 8 patients (26%) as a consequence of the disease. Posterior synechia, glaucoma, and white iritis were not observed in any patient. CONCLUSION: Ocular manifestations with potentially sight-threatening complications occur commonly in the CINCA/NOMID syndrome. The distinctive nature of these complications may assist the ophthalmologist in recognizing this rare disorder and distinguishing it from juvenile rheumatoid arthritis.

Abnormalities, Multiple↗

PubMed2004

A severe autosomal-dominant periodic inflammatory disorder with renal AA amyloidosis and colchicine resistance associated to the MEFV H478Y variant in a Spanish kindred: an unusual familial Mediterranean fever phenotype or another MEFV-associated periodic inflammatory disorder?

Familial Mediterranean fever (FMF) is an autosomal recessive disease characterized by recurring short attacks of fever and serositis. Secondary AA amyloidosis is the worst complication of the disease and often determines the prognosis. The MEFV gene, on chromosome 16p13.3, is responsible for the disease and around 30 mutations have been reported to date. Colchicine is the standard FMF treatment today, and prevents both attacks and amyloid deposition in 95% of patients. Here we describe a three-generation Spanish kindred with five family members affected by a severe periodic inflammatory disorder associated with renal AA amyloidosis and colchicine unresponsiveness. Clinical diagnosis of definite FMF disease was made based on the Tel-Hashomer criteria set. Genetic analyses revealed that all subjects were heterozygous for the new H478Y MEFV variant, segregating with the disease. In addition, mutations in the TNFRSF1A and CIAS1/PYPAF1/NALP3 genes, related to the dominantly inherited autoinflammatory periodic syndromes, were ruled out. However, the dominant inheritance of the disease, the long fever episodes with a predominant joint involvement, and the resistance to colchicine in these patients raise the question of whether the periodic syndrome seen in this kindred is a true FMF disease with unusual manifestations or rather another MEFV-associated periodic syndrome. We conclude that the new H478Y MEFV mutation is the dominant pathological variant causing the inflammatory periodic syndrome in this kindred and that full-length analyses of the MEFV gene are needed to obtain an adequate diagnosis of patients with clinical suspicion of a hereditary periodic fever syndrome, especially those from non-ancestral populations.

Adult↗

PubMed1985

Abnormal calcium and magnesium stores in erythrocytes and granulocytes from patients with inflammatory connective tissue diseases. Relationship to inflammatory activity and effect of corticosteroid therapy.

The mass fraction of Ca and Mg in isolated erythrocytes and granulocytes was measured using the nuclear microprobe technique. Conspicuous abnormalities were observed in cells from patients with rheumatoid arthritis and other inflammatory arthritides. Compared with the normal cellular content, total Ca was increased an average of 3 times in erythrocytes and 5 times in granulocytes. Total granulocyte Mg was increased about 3 times, whereas erythrocyte Mg was reduced to as much as 60% of normal. These abnormalities were less prominent or were absent in scleroderma patients, except for levels of granulocyte Ca, which were increased more than 3 times beyond normal in this patient group. A significant positive correlation was found between serum haptoglobin and erythrocyte or granulocyte Ca content among these patients, but not between haptoglobin and erythrocyte or granulocyte Mg values. During corticosteroid treatment, a significant increase in erythrocyte Mg and a significant reduction in erythrocyte Ca were noted, but normalization of these levels was not achieved. Granulocyte Ca was also significantly reduced, while granulocyte Mg remained unaltered. Serum levels of Ca and Mg were within normal ranges and were not influenced by corticosteroid therapy. The results indicate that at least Ca abnormalities in erythrocytes and granulocytes are associated with the intensity of the inflammatory process and that the amounts of Ca and Mg in these cells are influenced by potent antiinflammatory therapy.

Adrenal Cortex Hormones↗