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At least 19 recordsLinked to original sources
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↗
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↗
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↗
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

Histopathology of acute and chronic inflammation.

Inflammation, defined as local reaction to injury, is basically a homeostatic process-loop system with morphological and biochemical components. If this homeostatic loop is uncomplicated a normal situation is reached soon after injury. Morphologically different patterns of inflammation can appear, depending on the character and intensity of the injury. Furthermore, the contributions made by hyperaemia, exudation of fluid, infiltrates carrying inflammatory cells, and cell proliferation not only vary with the type of injury but also depend on the time after injury. Some of the histopathological changes can be seen as essential for the restoration of the normal situation, whereas others damage the tissue more than seems desirable. The morphological aspects of different types of inflammation are discussed in relation to the homeostatic nature of the inflammatory process.

Acute Disease↗
PubMedDate not supplied

Pathogenesis of chronic inflammation in experimental ferritin-induced arthritis. IV. Immuno-electron microscopic techniques in the study of articular collagenous tissues.

The earliest and most severe changes in articular collagenous tissues (ACT) occur within 24 hours of antigen challenge and are associated with and are possibly secondary to maximal immune complex deposition in ACT surfaces. The immuno-electron microscopic (immuno-em) staining characterizes the ferritin as aggregates with antibody and suggests its occurrence and deposition as a preformed immune complex. These data indicate a direct interaction between immune complexes and collagenous matrix which could relate to both antigen persistence and chronicity of the immune response. The changes described in this model have features in common with rheumatoid disease and suggest the potential for similar mechanisms of cartilage degradation.

Animals↗
PubMed2025

Aberrant TERT expression: linking chronic inflammation to hepatocellular carcinoma†.

Telomerase reverse transcriptase (TERT), the catalytic enzyme component of telomerase, plays multiple roles in cellular biology. Its canonical function is primarily associated with telomere maintenance and genomic stability. In addition, several studies revealed critical non-canonical extra-telomeric functions of TERT in various cellular processes, including cell proliferation and survival, DNA damage response, transcription, signal transduction, and metabolic regulation, both in normal and in cancer cells. Notably, TERT is aberrantly upregulated in more than 80% of hepatocellular carcinoma (HCC) cases, making it an important target in liver cancer research. However, due to the diversity and complexity of TERT's functions in vivo, the precise mechanisms by which TERT contributes to the initiation and progression of HCC remain unclear. A recent study published in The Journal of Pathology using the Alb-Cre;TertTg mouse model and clinical HCC samples addresses the role of TERT in hepatocarcinogenesis. The study demonstrates that TERT promotes cell cycle progression and hepatocarcinogenesis by enhancing NF-κB promoter activity and facilitating the ubiquitination of p21. Notably, absence of functional p53 accelerates liver tumor development in TERT transgenic mice. These findings further underscore the critical role of TERT in inflammation-driven hepatocarcinogenesis and provide new insights into its underlying mechanisms. © 2025 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland.

Telomerase↗