interstitial inflammation

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a localized protective response elicited by injury or destruction of tissues, which serves to destroy, dilute, or wall off both the injurious agent and the injured tissue. adj., adj inflam´matory.  

The inflammatory response can be provoked by physical, chemical, and biologic agents, including mechanical trauma, exposure to excessive amounts of sunlight, x-rays and radioactive materials, corrosive chemicals, extremes of heat and cold, or by infectious agents such as bacteria, viruses, and other pathogenic microorganisms. Although these infectious agents can produce inflammation, infection and inflammation are not synonymous.

The classic signs of inflammation are heat, redness, swelling, pain, and loss of function. These are manifestations of the physiologic changes that occur during the inflammatory process. The three major components of this process are (1) changes in the caliber of blood vessels and the rate of blood flow through them (hemodynamic changes); (2) increased capillary permeability; and (3) leukocytic exudation.

Hemodynamic changes begin soon after injury and progress at varying rates, according to the extent of injury. They start with dilation of the arterioles and the opening of new capillaries and venular beds in the area. This causes an accelerated flow of blood, accounting for the signs of heat and redness. Next follows increased permeability of the microcirculation, which permits leakage of protein-rich fluid out of small blood vessels and into the extravascular fluid compartment, accounting for the inflammatory edema.

Leukocytic exudation occurs in the following sequence. First, the leukocytes move to the endothelial lining of the small blood vessels (margination) and line the endothelium in a tightly packed formation (pavementing). Eventually, these leukocytes move through the endothelial spaces and escape into the extravascular space (emigration). Once they are outside the blood vessels they are free to move and, by chemotaxis, are drawn to the site of injury. Accumulations of neutrophils and macrophages at the area of inflammation act to neutralize foreign particles by phagocytosis.

Chemical mediators of the inflammatory process include a variety of substances originating in the plasma and the cells of uninjured tissue, and possibly from the damaged tissue. The major kinds of mediators are (1) vasoactive amines, such as histamine and serotonin; (2) plasma endopeptidases that comprise three interrelated systems, the kinin system that produces bradykinin, the complement system that produces proteins that interact with antigen--antibody complexes and mediate immunologic injury and inflammation, and the clotting system that increases vascular permeability and chemotactic activity for the leukocytes; (3) prostaglandins, which can reproduce several aspects of the inflammatory process; (4) neutrophil products; (5) lymphocyte factors; and (6) other mediators, such as slow-reacting substance of anaphylaxis and endogenous pyrogen.

Hormonal Response. Some hormones, such as cortisol, have an antiinflammatory action that limits inflammation to a local reaction while others are proinflammatory. Thus, the endocrine system has a regulatory effect on the process of inflammation so that it can be balanced and beneficial in the body's attempts to recover from injury.
Cellular changes in inflammation. 1, Margination of neutrophils brings these inflammatory cells in close contact with the endothelium. 2, Adhesion of platelets results in the release of mediators of inflammation and coagulation. Fibrin strands are the first signs of clot formation. 3, Pavementing of leukocytes is mediated by adhesion molecules activated by the mediators of inflammation released from platelets and leukocytes. RBC, red blood cells. From Damjanov, 2000.
acute inflammation inflammation, usually of sudden onset, marked by the classical signs of heat, redness, swelling, pain, and loss of function, and in which vascular and exudative processes predominate.
catarrhal inflammation a form affecting mainly a mucous surface, marked by a copious discharge of mucus and epithelial debris.
chronic inflammation prolonged and persistent inflammation marked chiefly by new connective tissue formation; it may be a continuation of an acute form or a prolonged low-grade form.
exudative inflammation one in which the prominent feature is an exudate.
fibrinous inflammation one marked by an exudate of coagulated fibrin.
granulomatous inflammation a form, usually chronic, attended by formation of granulomas.
interstitial inflammation inflammation affecting chiefly the stroma of an organ.
parenchymatous inflammation inflammation affecting chiefly the essential tissue elements of an organ.
productive inflammation (proliferative inflammation) one leading to the production of new connective tissue fibers.
pseudomembranous inflammation an acute inflammatory response to a powerful necrotizing toxin (such asdiphtheria toxin), characterized by formation on a mucosal surface of a false membrane composed of precipitated fibrin, necrotic epithelium, and inflammatory leukocytes.
purulent inflammation suppurative inflammation.
serous inflammation one producing a serous exudate.
subacute inflammation a condition intermediate between chronic and acute inflammation, exhibiting some of the characteristics of each.
suppurative inflammation one marked by pus formation.
toxic inflammation one due to a poison, e.g., a bacterial product.
traumatic inflammation one that follows a wound or injury.
ulcerative inflammation that in which necrosis on or near the surface leads to loss of tissue and creation of a local defect (ulcer).
Miller-Keane Encyclopedia and Dictionary of Medicine, Nursing, and Allied Health, Seventh Edition. © 2003 by Saunders, an imprint of Elsevier, Inc. All rights reserved.

in·ter·sti·tial in·flam·ma·tion

inflammation in which the inflammatory reaction occurs chiefly in the supportive fibrous connective tissue or stroma of an organ.
Farlex Partner Medical Dictionary © Farlex 2012

in·ter·sti·tial in·flam·ma·tion

(in'tĕr-stish'ăl in'flă-mā'shŭn)
Inflammation in which the inflammatory reaction occurs chiefly in the supportive fibrous connective tissue or stroma of an organ.
Medical Dictionary for the Health Professions and Nursing © Farlex 2012
References in periodicals archive ?
Combined all patients with various glomerular disorders, urinary ANXA1 protein levels positively correlated with the score of glomerular proliferation (r = 0.67, P < 0.001), interstitial inflammation (r = 0.54, P < 0.005), and glomerular sclerosis (r = 0.44, P < 0.001).
Alsuwaida, "Interstitial inflammation and long-term renal outcomes in lupus nephritis," Lupus, vol.
She later developed significant proteinuria, for which kidney biopsy was done showing nonproliferative morphology with patchy acute tubular injury and focal chronic interstitial inflammation. She was started with oral prednisolone and was kept on regular follow-ups with significant clinical improvements.
HandE and PAS stained histological sections were observed for tubular parameters (tubular degeneration, condition of the tubular basement membrane and presence of tubular cast) and interstitial parameters (interstitial inflammation and interstitial congestion).
An intraoperative biopsy of the transplanted kidney showed focal endothelialitis with minimal tubulitis (Banff t1) and minimal interstitial inflammation (Banff i0) (Figure 1).
Peribronchiolar, alveolar, and interstitial inflammation was apparent in all Cr(VI)-exposed mice, at all time points analyzed (Figure 2D-G).
[6] Last but not least, experimental studies have pointed out that the initial lesion appears to be crystal formation along the brush border of the proximal tubule, with eventual crystal deposition in collecting ducts and papillary interstitium, and eventual tubule obstruction, interstitial inflammation, and fibrosis.
Some cases of CHP have very little interstitial inflammation, but other cases have a readily discernible infiltrate of lymphocytes, plasma cells, and a few eosinophils (Figure 4, B), and the numbers of inflammatory cells are greater than one would expect in UIP/IPF, which should be quite paucicellular.
These changes were accompanied with disrupted brush borders and inclusion bodies in cytoplasm of tubular cells on PAS stained sections.11-13 Glomeruli were shrunken and there was increase in Bowman's space.14 On histopathological grading, extensive vascular congestion, hyaline casts, cortical vacuolar degeneration and interstitial inflammation were demonstrated.15 CsA had deleterious effects on foetal kidneys of albino mice.16
Therefore, corticosteroids and cyclophosphamide were given to inhibit interstitial inflammation and improve the prognosis.
Significant difference was observed between groups in percentages of tubular necrosis (pless than 0.001), tubular vacuolation (p less than 0.001), tubular casts (pless than 0.001), interstitial inflammation (pless than 0.001) and vascular congestion (p less than 0.001) between the groups (Table-1).
Interstitial inflammation, fibrosis and tubular atrophy are graded as mild moderate (2+), and severe (3+).

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