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PubMed1987

[Interferon gamma: a Janus-faced mediator in inflammation].

A survey is given of the immunomodulatory effects of interferon gamma (IFN-gamma) in inflammation. IFN-gamma influences the activity of macrophages, granulocytes, B-lymphocytes, suppressor-T-lymphocytes and natural killer cells as well as the production of prostaglandins and leukotrienes, bone resorption, collagen synthesis and expression of HLA class II antigens. Furthermore, the production of IFN-gamma in patients with chronic inflammatory diseases is described as well as the recent in vivo investigations concerning induction and inhibition of inflammation by IFN-gamma. Based on these investigations a hypothesis is presented which offers an explanation for the contradictory results concerning the effects of IFN-gamma in inflammation. According to this hypothesis IFN-gamma takes part in the elicitation of an inflammatory reaction. As soon as a high inflammation activity is reached the reaction is inhibited via a negative feedback. Therefore, exogenously applied IFN-gamma has a stimulating effect if inflammation activity is low. In contrary, IFN-gamma inhibits this reaction if activity is high. The consequences resulting from this dual mode of action for the treatment of different diseases with IFN-gamma are discussed.

B-Lymphocytes↗
PubMed1989

The prevalence and distribution of acute placental inflammation in uncomplicated term pregnancies.

The clinical relevance of histologic evidence of acute ascending intrauterine infection has been called into question by descriptions of "silent" chorioamnionitis. The described frequencies of silent chorioamnionitis in normal and abnormal pregnancies vary widely because of differences in the definition of a normal pregnancy, methods of placental examination, and pathologic criteria. Therefore, we examined placentas from 161 uncomplicated gestations for the presence and severity of acute inflammation in the amnion, chorion-decidua, chorionic plate, and umbilical cord using strict gross and microscopic protocols. Indicators of amniotic fluid infection, specifically umbilical cord inflammation, amnionitis, and inflammation within the chorionic plate were present in 0, 1.2, and 4% of the cases, respectively. Silent chorioamnionitis was rare. There was a statistical association between the presence of acute inflammation and the occurrence of labor at term. Methods of tissue sampling that included a more extensive examination of the site of membrane rupture resulted in an increased frequency of diagnosis of acute inflammation at the site of rupture in vaginal deliveries at term.

Acute Disease↗
PubMed1985

Inflammation induced by bacterial cell wall fragments in the rat air pouch. Comparison of rat strains and measurement of arachidonic acid metabolites.

Streptococcal cell wall fragments, suspended in phosphate-buffered saline, were injected into a preformed subcutaneous air pouch in rats. The advantage of the air pouch model is the capacity for quantitation of exudative, cellular, and proliferative responses and soluble mediators. Accumulation of pouch fluid containing many leukocytes occurred during the first 3 days. Granulation tissue separable from the surrounding subcutaneous tissue developed by 6 days. Immunofluorescence and immunoperoxidase staining showed the presence of cell walls in inflammatory cells both in pouch fluid and in pouch tissue. Histologic features of this inflammation included an acute exudative phase with a predominantly neutrophil infiltration followed by a chronic phase characterized by fibroblast proliferation, formation of blood vessels, and infiltration with mononuclear cells. The lining of the pouch before injection of cell wall developed morphologic features of synovial membrane, which became more evident during the chronic phase of induced inflammation. Outbred Sprague-Dawley and inbred Lewis rats developed more pouch fluid, cell numbers in the pouch fluid, and granulation tissue than inbred Buffalo rats. The arachidonic acid metabolites, prostaglandin E2 and leukotriene B4, were measured in the pouch fluid, and more of each was produced in the Lewis than in the Buffalo strain. These measurements of inflammation are consistent with the relative susceptibility of these strains to cell-wall-induced arthritis. This model of inflammation can be used in the examination of the regulatory mechanisms of evolving chronic inflammation.

Animals↗
PubMed1988

Granulomatous inflammation in pineal germinoma. A cause of diagnostic failure at stereotaxic brain biopsy.

We report four patients with pineal germinoma in whom the initial procedure for obtaining a tissue diagnosis was a stereotaxic biopsy. In all four cases, the biopsy showed granulomatous inflammation with epithelioid cells and lymphocytes. In one case, the granulomatous inflammation was accompanied by classical germinoma. Another case exhibited malignant cells considered nondiagnostic for a specific neoplasm. Two cases had no evidence of a malignant tumor; they were composed entirely of granulomatous inflammation. In two of the three cases where the diagnosis was not established by the first biopsy, a second stereotaxic biopsy showed pineal germinoma. Tissue obtained at resection in the third patient revealed large areas of granulomatous inflammation accompanying the germinoma. Immunoperoxidase stains for ferritin and placental alkaline phosphatase did not increase diagnostic yield. We conclude that a finding of granulomatous inflammation in a stereotaxic biopsy specimen of a pineal mass should suggest a diagnosis of germinoma, followed by sampling from several different target points within the lesion.

Adolescent↗
PubMedDate not supplied

Effect of experimental airway inflammation on bronchial hyper-responsiveness induced by Broncho-Vaxom in dogs.

We studied correlation between airway hyper-responsiveness induced by local exposure to a macrophage inductor Broncho-Vaxom and the development of airway inflammation in dogs. To detect airway inflammation, bronchoalveolar lavage and biopsy of airway mucosa were performed. The airway responsiveness was registered by capnograph measuring gas-exchange disturbances during obstructive reactions provocated by inhalation of various concentrations of acetylcholine aerosol. Broncho-Vaxom generated a protracted airway inflammation characterized by a slight and reversible increase in the number of neutrophils at 24 h after induction, and by a long-lasting influx of macrophages peaked about at the second week. The number of macrophages turned to initial levels 3 weeks later. Macrophages migrating to the bronchoalveolar surface were activated because peroxidase positivity and bearing C3b receptors of these cells increased gradually during the inflammatory process. Airway responsiveness measured at 3, 6 and 24 h after induction did not differ significantly from baseline values, but hyper-responsiveness was developed at 96 h using 0.5 and 1.0% acetylcholine aerosol (p less than 0.01 and p less than 0.001) during the non-purulent, macrophage-mediated inflammation. This situation modelled by Broncho-Vaxom induction is very similar to those observed in children with recurrent obstructive bronchitis. The results suggest that a macrophage-mediated inflammation caused by antigens, infections or pollutants may generate a long-lasting airway hyper-responsiveness.

Acetylcholine↗
PubMed1988

Transcriptional regulation of ceruloplasmin gene expression during inflammation.

Mixed sequence oligonucleotides were used to isolate a series of acute-phase human liver cDNA clones corresponding to the serum alpha 2-globulin ceruloplasmin. These clones were characterized, sequenced, and used to analyze changes in hepatic ceruloplasmin mRNA content during inflammation. In all species examined, hepatic ceruloplasmin mRNA content increased approximately 6-10-fold over control values within 24 h following the induction of inflammation. The mechanisms leading to this increase in hepatic ceruloplasmin mRNA content were studied following turpentine-induced inflammation in Syrian hamsters. Nuclear run-on assays demonstrated an increase in the relative rate of transcription of the ceruloplasmin gene within 3 h following induction, reaching maximum values by 18 h. Hepatic ceruloplasmin mRNA content increased 2-fold within 12 h following induction, reached maximum values by 24 h, and returned to control within 72 h. In contrast, serum ceruloplasmin concentration did not increase until 36 h, reached maximal levels by 120 h, and remained elevated for the course of the study. These data indicate that inflammation leads to a rapid increase in hepatic ceruloplasmin mRNA content. This increase is largely the result of increased ceruloplasmin gene transcription, but comparison of the relative rate of transcription and mRNA accumulation suggests that changes in ceruloplasmin mRNA turnover are also involved. In addition, translational and/or post-translational mechanisms must account for the observed changes in serum ceruloplasmin concentration seen during inflammation.

Animals↗
PubMed1987

Joint inflammation in mice induced by a MT4+ Lyt-2- T cell clone. Characteristics and the induction of flare-up reactions.

Joint inflammations were induced in mice by cloned MT4+ Lyt-2- T cells specific for methylated bovine serum albumin. This was done either by intra-articular or by i.v. administration of the cloned T cells, together with local injection of the antigen. Local rechallenge with methylated bovine serum albumin several weeks after waning of the joint inflammation caused a flare-up reaction. The inflammations were quantified by a 99mTc-uptake method and examined histologically. The arthritis induced by the cloned T cells showed aspects of a delayed type hypersensitivity reaction characterized by an intense infiltrate which resembles the inflammation in the human rheumatoid joint. The data presented show that joint inflammations can be induced by T cells only and that, after waning, reexposition to the original antigen can induce a flare-up reaction. The data suggest a central role of T cells in the induction and the exacerbations observed in rheumatoid arthritis.

Animals↗
PubMed1986

The clinical relevance of airway inflammation.

Inflammation forms an integral part of the normal defence mechanisms of the airways. Airway inflammation is therefore in essence beneficial, although prolonged exposure to noxious stimuli, overwhelming damage or insufficient control of the inflammatory process may lead to clinical disease. However, the factors contributing to the type and magnitude of airway inflammation, including the level at which damage occurs, the individual difference in sensitivity and inflammatory response to noxious stimuli and the evolution from acute to chronic inflammation, are insufficiently characterized. Clinical, pathological and experimental investigations clearly show that airway inflammatory disorders are heterogeneous. Mucus hypersecretion and bronchial hyperresponsiveness are different characteristics of airway diseases with distinct clinical manifestations and prognostic significance. Epidemiological studies have shown that bronchial hyperresponsiveness is associated with a worse prognosis in obstructive airway disease. Further efforts are needed to understand the impact of different parts of the airway inflammatory process on the physiological and clinical manifestations of airway diseases. Understanding the mode of action of existing and newly developed therapeutic agents on airway inflammation will teach us more about its role in these frequent disorders.

Adult↗
PubMed1986

Triggers of airway inflammation.

Most asthmatics have hyperresponsive airways. This makes them more sensitive than non-asthmatics to bronchoconstricting environmental exposures which, in their turn, may enhance responsiveness. Airway inflammation is considered to be a key determinant of airway hyperresponsiveness: the fact that chronic airway inflammation in cystic fibrosis does not lead to airway hyperresponsiveness of any importance indicates, however, that the role of airway inflammation is complex and incompletely elucidated. The main inducers of airway inflammation are viral infections, antigens, occupational stimuli and pollutants. Although exercise, airway cooling and hyper- or hypotonic aerosols are potent stimuli of bronchoconstriction, it is questionable if airway inflammation is involved in their mode of action. Each of the above-mentioned stimuli is discussed, with emphasis laid on the relation of symptoms to mechanisms.

Adult↗
PubMed1984

Inflammation due to intra-cutaneous implantation of stratum corneum.

Fragments of sterile heel callus and suspensions of human corneocytes were implanted or injected intra-cutaneously into flank skin of guinea pigs. A mixed cellular type of inflammation was produced characterized by the accumulation of polymorphonuclear leucocytes in the early stages and a more granulomatous picture in the later stages. Epithelial hypertrophy and follicular distortion with transepidermal elimination was a frequent accompaniment. Immunoglobulins and the complement component C3 were found scattered irregularly in the inflammation produced and were not thought to be important in the process. The inflammation produced closely emulated the changes observed in acne inflammation and after rupture of horn containing cysts. It is suggested that inflammation caused by the implantation of horn may be suitable for study of human skin disease in which horny debris is released into the dermis, such as acne.

Acne Vulgaris↗
PubMed1983

[Inflammation, immunity, hypersensitivity].

The conjugation between inflammation and hypersensitivity is analysed. In human pathology, these processes have been shown to be closely associated and to be in the cause-and-effect relationship, immunity being the connecting link between them: immune responses generated in inflammation for elimination of the injurious agent and reparation may, upon distortion of the inflammation kinetics, become responses of "sick immunity" or hypersensitivity responses leading to damage and immune inflammation. The problem of conjugation of inflammation and hypersensitivity with immunity covers a wide range of aspects of morphology, molecular biology, immunology, and genetics. The understanding of this conjugation will give an insight into immunopathology represented in all branches of the modern clinical science.

Complement System Proteins↗
PubMed1984

Pharmacological comparison of the immune and non-immune inflammations induced by picryl chloride and oxazolone in mice.

Picryl chloride applied to the ears of Swiss mice induced a clearcut primary irritation inflammation (maximal after 3 to 6 hr) and after contact sensitization performed 7 days before a delayed hypersensitivity reaction. Oxazolone produced only a weak primary irritation reaction. After contact sensitization in the same conditions as above, oxazolone induced an immune response that was already substantial 3 to 6 hr after the challenge and generally reached a maximum after 24 hr. We tried to alter these four types of inflammation (the primary irritation and delayed hypersensitivity to picryl chloride, and the 6-hr and 24-hr phases of hypersensitivity to oxazolone) by various types of compounds administered cutaneously or sytemically. Mepyramine, methysergide, cimetidine, disodium cromoglycate, phenylbutazone, and acetylsalicylic acid reduced to varying degrees after cutaneous application the primary irritation and the delayed hypersensitivity inflammation induced by picryl chloride. Methysergide was the only one of these drugs that on topical application clearly reduced the immune response to oxazolone (decrease in the 6-hr phase). After systemic administration, these same drugs had no effect on the four types of reaction. Both the corticosteroids tested (hydrocortisone acetate and desonide) reduced all the inflammations to various degrees and were always more active (particularly desonide) when applied topically than when administered systemically. On the other hand indomethacin, which inhibited all types of inflammation, was more active when administered systemically. Study of the kinetics and trials of pharmacological modulation of the various reactions induced by picryl chloride and oxazolone in Swiss mice provided evidence of differences in behavior between the two agents.

Adrenal Cortex Hormones↗
PubMed1983

[Allergic inflammation].

Current ideas of allergic inflammation reflected in the concept of immune inflammation are described. This concept considers immune inflammation to be an immune response mediated by a certain immunity reaction which gives the inflammation a number of qualitative and quantitative differences. The nature of the differences allows allergic (immune) inflammation to be evaluated as a biologically expedient type of defence-adaptative reaction in which the inflammatory response is optimally expressed owing to the participation of immunological mechanisms.

Eosinophils↗
PubMed1984

[Effect of a weak magnetic field on the course of an acute inflammation in the rat].

To determine the influence of weak magnetic field on the development of inflammations, a non-specific acute inflammation was induced in rats by subcutaneous injection of sterile SEPHADEX-gel in the lower dorsal quadrants. The magnetic field applied had a strength of 10 Gauss (equivalent to 20 times the magnetic field of the earth), rectangular curve and a frequency of 10 Hz. Following a field exposure of 2 and 3 days, cytological and biochemical analyses of the blood and inflammatory exudate were performed. Parameters were leucocytes and proteins in the blood and in the focus of inflammation as well as blood electrolytes. The protein values in the focus of inflammation of the control animals remained unchanged on the second and third day whereas in the animals exposed to the magnetic field, they increased from the second to the third day. In the blood similar effects could be seen, but they were not as pronounced. We conclude from these data that the magnetic field causes an increased exudation of serum proteins in the focus of inflammation. The cellular component remains unchanged.

Acute Disease↗
PubMed1980

Depletion of hepatic antioxidants during granulomatous inflammation in the rat and local anti-inflammatory effects of free radical scavengers.

Changes in hepatic oxidative events have been studied during extrahepatic granulomatous inflammation in the rat, together with the local anti-inflammatory effects of scavengers of reactive oxygen species. During remote localized inflammation in the rat, we observed increased hepatic lipid peroxidation and reduced hepatic levels of protecting substances such as ascorbic acid, catalase and reduced glutathione, the specific substrate for the peroxide-metabolizing enzyme, glutathione peroxidase. The levels of superoxide dismutase did not alter significantly during the period of investigation (7 days). The half-life of aminopyrine was longer in rats with a stronger inflammatory response. In addition, catalase and the anti-oxidants, alpha-tocopherol and propyl gallate, inhibited granuloma development on local injection during the acute phase inflammation. Superoxide dismutase alone was devoid of anti-inflammatory effects, but markedly enhanced the effect of catalase. Scavengers of hydroxyl radicals and of singlet oxygen failed to display anti-inflammatory activity. The results indicate that peroxides may act as mediators of inflammation and that increased lipid peroxidation is not limited to the site of inflammation.

Animals↗
PubMed1994

Inositol polyanions. Noncarbohydrate inhibitors of L- and P-selectin that block inflammation.

Selectins are cell adhesion molecules known to support the initial attachment of leukocytes to inflamed vascular endothelium through their recognition of carbohydrate ligands such as the tetrasaccharide sialyl Lewisx (Neu5Ac alpha 2-3Gal beta 1-4(Fuc alpha 1-3)GlcNAc-). In the present study, we describe the inhibition of L- and P-selectin function by inositol polyanions, simple 6-carbon ring structures that have multiple ester-linked phosphate or sulfate groups. In a purified component competition assay, binding of L- and P-selectin-Ig fusion proteins to immobilized bovine serum albumin-sialyl Lewisx neoglycoprotein was inhibited by inositol hexakisphosphate (InsP6, IC50 = 2.1 +/- 1.4 microM and 160 +/- 40 microM), by inositol pentakisphosphate (InsP5, IC50 = 1.4 +/- 0.2 and 260 +/- 40 microM), and by inositol hexakissulfate (InsS6, IC50 = 210 +/- 80 microM and 2.8 +/- 0.9 mM); E-selectin-Ig binding was unaffected. Inositol polyanions diminished the adhesion of LS180 colon carcinoma cells to plates coated with L- and P-selectin-Ig but not with E-selectin-Ig. Inositol polyanions blocked polymorphonuclear leukocyte (PMN) adhesion to COS cells expressing recombinant transmembrane P-selectin but not to those expressing E-selectin. In addition, inositol polyanions diminished PMN adhesion to activated endothelial cells under rotation-induced shear stress, a process known to require L-selectin function. In vivo, the effects of inositol polyanions were studied in two murine models of acute inflammation. Intravenously administered InsP6 (two doses of 40 mumol/kg) inhibited PMN accumulation in thioglycolate-induced inflammation (55 +/- 10% inhibition) and in zymosan-induced inflammation (61 +/- 4% inhibition). InsP5 and InsS6 also inhibited inflammation in these models, although higher doses were required for InsS6. In conclusion, inositol polyanions are noncarbohydrate small molecules that inhibit L- and P-selectin function in vitro and inflammation in vivo.

Animals↗
PubMed1994

Expression of murine VCAM-1 in vitro and in different models of inflammation in vivo: correlation with immigration of monocytes.

VCAM-1 (vascular cell adhesion molecule-1) is a cytokine-inducible adhesion molecule which is known to mediate adhesion of mononuclear cells to endothelial cells in vitro via binding to the integrin VLA-4 (very late antigen-4). To further elucidate the role and regulation of VCAM-1 in vivo, we compared in vitro and in vivo expression of VCAM-1 in response to cytokines and investigated immunohistochemically the expression of VCAM-1 in three murine models of experimental inflammation. These models differed with regard to the pathogenetic mechanism and the subsequent infiltrate: allergic contact dermatitis (ACD) to DNFB as a T cell-controlled, DTH type of inflammation, cutaneous infection with Leishmania major as a chronic granulomatous inflammation and the cauterized cornea as a model for acute inflammation. VCAM-1 was found to be markedly enhanced on vascular endothelia in all types of inflammation and after subcutaneous administration of LPS and TNF-alpha. Administration of IL-4, however, failed to induce VCAM-1 both in vivo and in vitro. The increased VCAM-1 expression in the inflammatory models correlated with the appearance of infiltrating monocytes/macrophages. A concomitant influx of CD4-positive/CD8-positive lymphocytes was only observed in ACD and Leishmaniasis.

Animals↗
PubMed1994

Antiinflammatory effect of flavonoids in the natural juice from Aronia melanocarpa, rutin and rutin-magnesium complex on an experimental model of inflammation induced by histamine and serotonin.

The antiinflammatory effects of the anthocyane flavonoids in the natural juice from Aronia melanocarpa and of rutin-magnesium complex, the water-soluble derivative of rutin were studied in comparison with rutin. Two experimental models of inflammation were used. Inflammation of rat hind paw was induced either by 0.5% solution of histamine or by 0.01% solution of serotonin. The swelling of the rat paw was measured oncometrically by a pletismometer. The results showed that the anthocyane flavonoids from the natural juice of Aronia melanocarpa exerted more pronounced effects as compared to rutin in both models of inflammation. The rutin-magnesium complex did not exhibit any antiinflammatory activity against histamine-induced inflammation. Its effects against serotonin-induced inflammation were comparable to those of rutin.

Animals↗