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Results for “chronic inflammation”

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At least 19 recordsLinked to original sources
PubMed1978

The incidence and clinical relevance of chronic inflammation in the pancreas in autopsy material.

In 394 consecutive autopies, tissue from the body of the pancreas showed chronic inflammation in 52 cases (13%); 32 were mild, 11 moderate and 9 severe. Only two of these cases had the clinical diagnosis chronic pancreatitis. The incidence of inspissated plugs of protein in the ducts, dilated ducts and acinar ectasia was significantly higher when chronic inflammation was present. There was a significant higher incidence of chronic inflammation in the pancreas in patients with diabetes mellitus. No significant correlation was noted between chronic inflammation in the pancreas and cholelithiasis, previous cholecystectomy, peritonitis, gastric and duodenal ulcer, abdominal operations, ascites and liver metastases.

Adult↗
PubMed1975

Human monocytopoiesis in acute and chronic inflammation.

Monocytopoiesis was analyzed in patients with severe, acute inflammations induced by surgical interventions as well as in others with mild, chronic inflammations in connection with gastric or duodenal ulcers. The state of acute inflammation was assumed to be associated with a high and steeply rising monocyte demand as opposed to the constant and relatively small monocyte recruitment in chronic inflammation. In chronic mild inflammatory reactions DNA synthesis activity of promonocytes was increased by a factor of about two; the promonocyte pool was normal. In patients who underwent surgical operations changes in the following parameters were observed during the first 15 h after start of surgery: (1) average increase in 3H-TDR labelling index by 38%; (2) average enlargement of promonocyte pool by 34%, (3) and relase of immature cells from the bone marrow into the blood. Increase in DNA synthesis activity as well as expansion of the promonocyte pool causes an enhanced monocyte production rate. The 'shift to the left' in monocyte egress is equivalent to a reduced stem-cell-to-blood transit time. These variations permit short-term adaptation of monocytopoiesis to varying demands.

Acute Disease↗
PubMed1976

The macrophage as a secretory cell in chronic inflammation.

Although it is clear that macrophages are always present at sites of chronic inflammation their contribution to the evolution of these lesions is not well understood. In vitro studies have shown that macrophages secrete a variety of products on exposure to different stimuli. These include hydrolytic enzymes, active at acid or neutral pH, with known capacity for degrading tissue constituents. Lysosomal acid hydrolases are released from viable cells over a prolonged period of time by various agents known to cause, or are associated with, chronic inflammation. These agents may be nonimmunogenic substances, such as carrageenan and asbestos, which interact directly with macrophages or alternatively the products of immune reactions involving either B or T lymphocytes. These lymphocyte products include immune complexes of certain composition and the secreted products of T lymphocytes stimulated by nonspecific mitogens or specific antigens. In marked contrast biologically inactive substances such as latex particles or digestible substrates such as erythrocytes do not induce the selective release of acid hydrolases from macrophages. It is clear that alghough macrophages secrete abundant amounts of neutral proteinases under certain conditions this release does not occur necessarily during the release of acid hydrolases induced by inflammatory agents. The role played by acid and neutral hydrolases secreted by macrophages during the various stages of chronic inflammatory responses remains to be clarified.

Animals↗
PubMed1978

Relationship between lymphocyte emigration and vascular endothelium in chronic inflammation.

Small blood vessels within areas of chronic inflammation which contain large numbers of lymphocytes develop unusually thick walls. Combined histological and electron microscope study shows that the thickening is due to hypertrophy of endothelial cells which come to resemble the endothelium of post-capillary venules in lymphoid tissue. Vessels of this type have been found in experimental granulomas induced by injection of Freund's adjuvant or killed tubercle bacilli and in human biopsy material from cases of rheumatoid arthritis and Hashimoto's disease of the thyroid. Comparison with the developing Peyer's patch in young rats shows that the unusual vessels in granulomas are very similar in endothelial cell size, pattern of distribution, extent of lymphocyte migration and degree of carbon leakage to post-capillary venules of the immature Peyer's patch. Study of the time at which lymphocytes appear in large numbers within the granuloma or developing Peyer's patch and the time at which thickened vessels are first seen suggest tha the endothelial changes are a consequence and not a cause of lymphocyte emigration. The stimulus to endothelial hyperthrophy appears to be massive sustained migration of lymphocytes, but the functional significance of this change in vascular structure is not clear.

Animals↗
PubMed1979

Vascular permeability in the rat gingiva. A model of vessel response in chronic inflammation.

The vascular permeability of the vessels of clinically normal gingiva of rats was studied using the colloidal carbon technique. The connective tissue situated underneath the keratinised epithelium was normal, but that subjacent to the non-keratinised epithelium showed some degree of chronic inflammation and as a rule the vessels of the area exhibited increased vascular permeability. In the buccal gingiva the vessels labelled with carbon form loops situated 200 micrometers below the marginal gingiva, while in the interdental gingiva the altered vessels are just below the superficial epithelium. On electron microscopy the vessels in the inflamed areas showed many open endothelial junctions, and also pseudo-fenestration, and endoplasmic vesicles full of carbon. Little is known about vascular changes in chronic inflammation, and the rat gingiva seems to be a suitable model for their study.

Animals↗
PubMed1977

Reduced exudation and increased tissue proliferation during chronic inflammation in rats deprived of endogenous prostaglandin precursors.

Two models of chronic inflammation were studied in rats deprived of endogenous precursors of prostaglandins by feeding the animals on essential fatty acid deficient (EFAD) food. During kaolin-induced pouch-granuloma, exudate production was markedly reduced in EFAD rats, when compared with normal animals. The exudates from normal rats contained large amounts of PGE, but in the exudates from EFAD rats the amount of PGE was very markedly reduced. Similarly, with carrageenan-impregnated polyether sponges, the exudative component of inflammation was reduced in EFAD rats. However, the proliferative component was significantly increased, particularly in relation to the stunted growth of EFAD rats. Sponge exudates from EFAD rats contained fewer leucocytes than those from normal animals but the fall in leucocyte count was much smaller than the very marked reduction in PGE activity. EFAD rats also exhibited a significant increase in adrenal weights. The results are discussed in the light of the ambivalent (pro- or anti-inflammatory) role of endogenous PGS. It appears that, in the proliferative phase of inflammation, the anti-inflammatory role of PGs is more dominant.

Animals↗
PubMed1979

Vitamin E-induced chronic inflammation in rats.

Sub-plantar injection of vitamin E (VE) oil produces a highly localized, chronic inflammation which is sustained for at least 8 weeks. As a result of studies using mediator inhibitors and depletors, it appears that histamine, serotonin, kinins, and prostaglandins may be involved in at least the early response to VE. This early phase is dominated by a massive influx of neutrophils, with the reaction rapidly progressing to a sustained mononuclear cell pathology. Results of studies in leucopenic rats suggest that edema formation and accumulation of white cells may be dissociable, although at this time it is not possible to conclude that edema can occur in the absence of cells since profoundly leucopenic rats are still able to locally mobilize polymorphonuclear cells in response to VE. Vitamin E-induced inflammation, produced under the conditions described, can be effectively suppressed by corticosteroids but seems relatively insensitive to the action of most non-steroidal anti-inflammatory agents tested.

Adrenal Glands↗
PubMed1977

[Functional and structural changes in the adrenal cortex of rabbits under conditions of chronic inflammation of the prostate gland].

Investigation of the state of the rabbit adrenal cortex under conditions of depression of the incretory activity of the testicles resulting from chronic inflammation of the prostate showed progressive hyperplasia of the reticular zone of the adrenal cortex; as to the glomerular zone, it failed to display any marked pathological changes, and the fascicular zone demonstrated some signs of hypoplasia. Thus, the normal or elevated androgen excretion observed in the experimental male rabbits, was provided by an intensified activity of the reticular zone of the adrenal cortex, despite a decrease in testosterone biosynthesis in the testes.

Adrenal Cortex↗
PubMed1978

The role of macrophage activation in chronic inflammation.

The macrophage is the characteristic cell type in chronic inflammatory reactions, in the rheumatoid synovium, as in other sites. When macrophages are activated, considerable synthesis of enzymes and other proteins occurs. Macrophages can be activated by (i) products of activated lymphocytes, (ii) immune complexes and (iii) the complement cleavage product C3b. Among the many consequences of macrophage activation are (i) secretion of hydrolytic enzymes, (ii) cleavage of C3 into C3a, which is cytolytic, and C3b, (iii) production of tissue thromboplastin, a powerful procoagulant, and (iv) formation of polyamine oxidase, which in the presence of appropriate substrates generates factors that lyse or limit the proliferation of tumour cells, lymphocytes and micro-organisms. The relevance of these observations to the pathogenesis of chronic inflammatory reactions is discussed.

Animals↗
PubMed1979

Suppression of acute and chronic inflammation in tumor-bearing rats.

Both acute and chronic cellular inflammatory reactions were suppressed in rats bearing malignant tumors. Inhibition of the acute inflammatory reactions was demonstrated in immune complex-induced vasculitis and in the accumulation of leukocytes in subcutaneously implanted polyvinyl sponges. Suppression of chronic inflammatory reactions was demonstrated in delayed type hypersensitivity skin reactions. In spite of these suppressed reactions, dermal reactivity to vasopermeability mediators was not diminished. Neither serum complement levels nor numbers of circulating leukocytes were depressed in animals with tumors. Suppression of inflammatory reactions was paralleled by a leukotactic defect which involved both neutrophils and monocytes. This defect could be ascribed to an abnormality in the serum that rendered both cell types leukotactically defective.

Animals↗
PubMed1977

The selective release of lysosomal acid hydrolases from mouse peritoneal macrophages by stimuli of chronic inflammation.

The paralelism between the capacity of various agents to elicit chronic inflammatory responses in vivo and to induce the selective release of lysosomal enzymes from cultures of mouse peritoneal macrophages in vitro is discussed. Zymosan elicits an intense inflammatory response when injected i.m. in mice. Chrysotile asbestos produces a response of a similar nature and intensity as is seen with zymosan, while injections of acid-leached asbestos and polystyrene latex are not followed by inflammation. It is also shown that zymosan and asbestos induce a dose-dependent increase in the total enzyme activity of an inflamed muscle. On the other hand latex and acid-leached asbestos caused no significant increases in lysosomal enzyme levels. Agents eliciting inflammatory responses, such as zymosan and chrysotile asbestos induce a selective release of acid hydrolases from cultured macrophages; in contrast agents lacking the capacity to induce inflammation, such as latex and acid-leached chrysotile asbestos, do not induce the release of lysosomal enzymes from cultured macrophages.

Animals↗