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PubMed1979

Interaction of salicylates and other non-steroidal anti-inflammatory agents in rats as shown by gastro-ulcerogenic and anti-inflammatory activities, and plasma concentrations.

The interaction of salicylates and other non-steroidal anti-inflammatory drugs was studied in rats. Concurrent oral administration of sodium salicylate (SS) or salicylic acid (SA) and indomethacin (IND) significantly reduced the gastro-ulcerogenicity and the plasma concentrations of IND. Acetylsalicylic acid (ASA) failed to do so. IND had no significant influence on plasma concentrations of SA. Simultaneous administration of SS and IND intraperitoneally or subcutaneously showed the same pattern of interaction as for oral administration. Concurrent oral administration of SS and IND exerted similar anti-inflammatory activity as the single drugs. SS significantly antagonized the ulcerogenicity of ibuprofen and tended to antagonize the ulcerogenic activity of ASA, phenylbutazone, tolfenamic acid and naproxen. The results suggest that in rats SS and SA (but not ASA) interact with IND concerning both gastro-ulcerogenicity and plasma concentrations of IND (but not of SA) and that the interaction is systemic in nature. We propose that the ulcerogenic interaction might be explained partly by the reduced IND plasma concentrations and partly by a weaker inhibition by SS of the prostaglandin system in the rat stomach.

Administration, Oral↗
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↗
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↗
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↗
PubMed1976

Inflammatory cells in solid murine neoplasms. I. Tumor disaggregation and identification of constituent inflammatory cells.

Mechanical and enzymatic methods of disaggregating tumors were studied with the goals of (1) minimizing cell losses while (2) maintaining functional and surface membrane markers needed to objectively identify inflammatory cells (IC)1 in resultant suspensions. Application of the principles and methods described makes accurate estimation of the percentage of each IC type present in neoplasms possible for the first time. Compared to purely mechanical means of disaggregating tumors, all enzyme mixtures tested markedly increased yields of viable cells/g neoplasm. Best results were obtained with a combination of collagenase and a protease of broader substrate range (alpha chymotrypsin, papain, pronase or trypsin). The combination of enzymes that gave the highest yields with the least effect on inflammatory cell markers was trypsin, collagenase and DNAse (TCD). Because mechanical injury appeared to be the greatest single cause of cell loss (the enzymes themselves had little direct effect), potential sources were identified and either eliminated or minimized. With TCD, depending on the tumor system, cell recovery (measured as DNA recovered in cell suspensions) was as high as 50% and yields were as much as 6.9 X 10(8) viable cells/g tumor. Complete disaggregation was not required to obtain representative IC populations from tumor fragments. Neutrophils, eosinophils and mast cells from disaggregated neoplasms were counted in Giemsa stained cytocentrifuge preparations based on their unique morphologic appearances. Macrophages were identified by their capacity to phagocytose zymosan, a function which proved highly resistant to the effect of enzymes. Flourescent microscopic identification of brain associated thymus antigen (BATA) allowed quantification of T lymphocytes, since this marker was virtually unchanged by enzyme exposure. Surface immunoglobulin (Ig) was stripped from B lymphocytes most rapidly by pronase and chymotrypsin, slowly by trypsin and papain, and not at all by collagenase. Ig positive cells therefore could be quantified in suspensions generated by collagenase or very short (20 min) exposure of fragments to trypsin.

Animals↗
PubMed1975

Inflammatory pseudotumors (inflammatory fibrous polyps) of the esophagus. A clinicopathologic study.

When they involve the gastrointestinal tract, inflammatory pseudotumors, composed of inflamed fibrous and granulation tissue, produce localized, frequently polypoid, masses. These rare lesions have been described in the stomach, small intestine, and colon. Only two have been previously reported in the esophagus. In this paper, 4 cases of inflammatory pseudotumor involving the esophagus are presented. These lesions usually occur in the esophagus as raised, occasionally pedunculated, masses and may be mistaken on radiologic examination and in the operating room for a neoplasm, usually a leiomyoma. Theories concerning pathogenesis of these lesions are considered and the differential diagnostic criteria are discussed.

Aged↗
PubMed1992

Markers of inflammatory activation: upregulation of complement receptors CR1 and CR3 on synovial fluid neutrophils from patients with inflammatory joint disease.

Expression of the C3 receptors CR1 and CR3 was investigated on neutrophils from paired peripheral blood and synovial fluid samples from 34 patients with inflammatory joint disease (21 patients with rheumatoid arthritis (RA) and 13 patients with other articular diseases (OAD)). Using monoclonal antibodies (anti-CD35, anti-CD11b) and immunofluorescence flow cytometric analyses the percentages of positively labeled cells and the relative fluorescence intensities (as a measure of receptor number) were determined. CR1 and CR3 were found to be present on the majority (> 85%) of circulating neutrophils from normal subjects, RA and OAD patients, and on synovial fluid neutrophils from both patient groups. A strong correlation between neutrophil CR1 and CR3 expression was observed in peripheral blood samples from normal subjects (r = 0.81; P = 0.001), RA (r = 0.79; P = 0.001), and OAD patients (r = 0.83; P = 0.001); in each case the levels of CR3 expression were approximately twice those recorded for CR1. Both CR1 and CR3 expression was upregulated on synovial fluid neutrophils compared with that observed on the corresponding peripheral blood cells. Mean percentage increases observed were: RA patients: CR1, 16.5% (P < 0.001) and CR3, 28.7% (P < 0.001); and OAD patients: CR1, 4.1% and CR3, 26.9% (P = 0.001). Correlation of serum and synovial fluid IL-6, IL-8, and immune complex levels with neutrophil CR1 and CR3 expression failed to demonstrate any significant relationship between the concentrations of these soluble factors and receptor expression. Upregulation of CR1 and CR3 receptors, reflecting neutrophil activation within the inflamed joint, is a consistent finding in patients with inflammatory arthropathies.

Adult↗
PubMed1992

Metabolic activity in inflammatory and non-inflammatory aneurysms of the abdominal aorta.

Inflammatory aneurysms of the abdominal aorta (IAA) comprise 10-15% of all aortic aneurysms (AA) but their aetiology and pathogenesis are obscure. Destruction of mural elastin is a prominent feature of IAA, and both increased elastolysis and decreased inhibition of elastolysis have been implicated. In order to study these factors, we have examined the peripheral blood of three groups of patients; 15 with inflammatory aortic aneurysms (IAA), 61 with simple aortic aneurysms (SAA) and 35 with aorto-iliac occlusive disease (OD). In all cases, alpha-1-anti-trypsin (A-1-AT), alpha-2-macroglobulin (A-2-MG), elastase inhibitory activity (E.I.A.), elastase-anti-trypsin complex, C-reactive protein (CRP), caeruloplasmin (CP) and plasma viscosity were measured. Patients with IAA had a significantly higher plasma viscosity (Mann-Whitney, p less than 0.05), E.I.A. (Mann-Whitney, p less than 0.01) and levels of A-1-AT, CRP, CP and elastase/anti-trypsin complex (Mann-Whitney, all p less than 0.05) than patients in the other two groups. There was no difference in the levels of A-2-MG between any of the groups. This study refutes the theory that reduced inhibition of elastase activity predisposes to the formation of SAA. In patients with IAA, raised marker levels indicate ongoing destruction of elastin, and suggest a difference in pathogenesis between IAA and SAA. The study also suggests that IAA are highly active metabolically, as opposed to the more degenerative SAA.

Acute-Phase Proteins↗
PubMed1977

Lysozyme activity in cerebrospinal fluid. Studies in inflammatory and non-inflammatory CNS disorders.

Lysozyme activity was measured in cerebrospinal fluid (CSF) from 114 patients with inflammatory (bacterial and serous meningitis, polyradiculitis, encephalitis) and non-inflammatory (multiple sclerosis, CNS tumors, cerebral vascular diseases) CNS diseases. Highly elevated values were found consistently in patients with bacterial meningitis. Elevated values were found also in patients with encephalitis, polyradiculitis, multiple sclerosis and CNS tumors, but a considerable overlapping between these groups and normal controls precludes the use of CSF lysozyme measurements as a diagnostic aid in the latter disease groups. Simultaneous measurements of lysozyme, albumin and IgG in CSF and serum suggested that the mechanism for increased CSF lysozyme values in bacterial meningitis is mainly a breakdown of the blood/brain barrier, whereas the increased CSF lysozyme values in the remaining groups of patients are more likely caused by production of lysozyme by cells within the meninges (neutrophilic granulocytes, monocytes?).

Blood-Brain Barrier↗
PubMed1992

Immunohistochemical analysis of synovial membranes from inflammatory and non-inflammatory arthritides: scarcity of CD5 positive B cells and IL2 receptor bearing T cells.

Rheumatoid Arthritis (RA) synovial membranes were examined by single and dual immunohistological techniques with a number of monoclonal antibodies against lymphocyte and macrophage related antigens. CD4 positive T lymphocytes frequently expressed MHC Class II antigens and were found in sublining collections in close association with activated macrophages as well as B lymphocytes. CD8 positive T cells surrounded these collections as well as being scattered throughout the membrane and also frequently expressed MHC Class II antigens. IL2 receptor (IL2r) expression on T cells and CD5 expression on B cells were rarely seen in these synovial membranes. Similar immunohistological architecture was found in synovial membranes from patients with psoriatic arthritis (PA) and Reiter's Syndrome (RS). Normal synovium contained few T cells, with few cells expressing MHC Class II antigens. Synovium from osteoarthritis (OA) patients also demonstrated similar immunohistological changes to those found in inflammatory arthritides, suggesting that there are only quantitative rather than qualitative differences between the synovial membrane immunohistological architecture from patients with inflammatory and noninflammatory arthritides.

Adult↗
PubMed1975

[Pharmacological study of 9 alpha-fluoro-11 beta, 17, 21-trihydroxy-16 beta-methylpregna-1, 4-diene-3,20-dione-17-benzoate (betamethasone-17-benzoate, MS-1112), a local anti-inflammatory agent. (1). Its anti-inflammatory and other pharmacological properties].

The anti-inflammatory activity and the other pharmacological properties of MS-1112, a new steroid compound, were examined and compared with other glucocorticoid analogues such as hydrocortisone acetate (Hydr), betamethasone 17-valerate (Val) and dexamethasone (Dexa). Systemically administered MS-1112 and glucocorticoids had a significant effect in inhibiting rat paw edema induced by various phlogistic stimulations and increasing vascular permeabilities and granuloma formation by cotton pellet or granuloma pouch. The order of those inhibiting activity was, in general, Dexa greater than MS-1112 greater than Val greater than Hydr. Concomitantly, Xthymolysis and adrenal weight suppression and reduced rate of body weight gain after multiple systemical administration were also observed. Locally administered MS-1112 caused an inhibiting activity, without systemic side-effects. This activity was approximately 3 to 5 times more potent than that of Dexa in rat carrageenin paw edema and cotton pellet granuloma. MS-1112 was less active than Dexa in glycogen liver deposition activity and in the depression of plasma level of corticosterone but more active than Val and Hydr. In the dose administered, MS-1112 had neither androgenic and anabolic nor estrogenic and anti-estrogenic activity. From this data, it concluded that MS-1112 is a very potent agent applicable regarding permeability and retention of steroids in a local site.

Administration, Topical↗
PubMed1992

Inflammatory cells and mediator release during ragweed challenge: correlation between histamine content in nasal secretions and appearance of inflammatory cells.

The early and late phase responses in the nasal tissues exhibit release of inflammatory mediators and a mixed cellular influx in separate nasal challenges. To explore this phenomenon further, histamine concentration was determined along with characterization of cell influx during dose-dependent ragweed challenges. Ten subjects with allergic rhinitis underwent two unilateral nasal lavages using incremental 3-fold concentrations of short ragweed. Low doses of ragweed (0.016 to 0.114 units Amb a I) rarely induced cell influx (1/18 challenges), whereas moderate doses (0.432 to 1.3 units Amb a I) caused cell influxes in 7/18 and high doses (3.39 to 11.7 units Amb a I) resulted in cell influxes in 8/17. The eluent contained greater than 50% neutrophils in seven challenges; greater than 50% eosinophils in three; and a mixed pattern in six. There was a significant association between the dose of antigen and the level of histamine. Challenges with an eosinophilic influx tended to be associated with higher concentrations of histamine than neutrophilic influxes. Similar to the immediate skin response, the early allergic response in the nose demonstrated a cell influx with release of histamine. Nasal cellular inflammation therefore can occur within minutes of allergen exposure.

Adult↗
PubMed1978

[Variation of the inflammatory response of an autologus implant function and viability: mixed and unilateral inflammatory response].

The behaviour of an autologous grafted implant depends upon its viability. In our study, pericardial implants were used as cardiac valves. Results showed that when using fresh live pericardium, an inflammatory response developed destroying it within 8 days. When implants cells were killed without alteration of their antigenicity--in order to prevent rejection--cellular growth and neovascularisation from implantation site occurred leading to a secondary live graft. Controlled killing of the implant seems to be an essential step in order to get live grafts.

Animals↗
PubMed1992

Studies of gut mucosal protein synthesis in a non-steroidal anti-inflammatory drug (NSAID) model of inflammatory bowel disease.

The extent to which defects in protein synthesis occurred in an experimental indomethacin induced rat model of nonsteroidal enteropathy has been examined. Male rats (nine) were fed indomethacin (8 mg/kg/day) for three days mixed with a powdered form of chow. The control group of rats (nine) were fed the same diet for three days without indomethacin. After the feeding period, both groups were fed a normal solid diet for four days. At the end of this period, the fractional rates of intestinal protein synthesis was determined by the 'flooding dose' technique. The mucosal protein, RNA and DNA contents in the proximal ileum of animals with enteropathy were not significantly different from controls (p greater than 0.05). Experimental enteropathy induced selective increases in the fractional rates of protein synthesis (26% increase, p less than 0.03) and RNA activities (23% increase, p less than 0.04). There were no significant changes in any of these variables in the duodenum (p greater than 0.05 in all instances). These changes may partly reflect the activity of those processes responsible for the pathogenic changes in NSAID enteropathy.

Animals↗