Inflammation polymorphonuclear leukocytes

Figure 36-2. Sites of action of some anti-inflammatory drugs in a gouty joint. Synoviocytes damaged by uric acid crystals release prostaglandins (PGs), interleukins (ILs), and other mediators of inflammation Polymorphonuclear leukocytes (PMNs). macrophages, and other inflammatory cells enter the joint and also release inflammatory substances, including leukotrienes (eg, LTB ), that attract additional inflammatory cells. Colchicine acts on microtubules in the inflammatory cells. NSAIDs act on cyclooxygenase-2 in all of the cells of the joint.

Levine, P.H., Hardin, J.C., Scoon, K.L. and Krinsky, N.I. (1981). Effect of corticosteroids on the production of superoxide and hydrogen peroxide and the appearance of chemiluminescence by phagocytosing polymorphonuclear leukocytes. Inflammation 5, 19-27. 

Biemond, P., Van Eijk, H.G., Swaak, A.J.G. and Koster, J.F. (1984). Iron mobilization from ferritin by superoxide derived from stimulated polymorphonuclear leukocytes. Possible mechanism in inflammation diseases. J. Clin. Invest. 73, 1576-1579. 

Moreover,bioactive lipids maybe considered dual messengers they modulate cell functions as messengers and they become part of the response of the nervous tissue to injury, broadly referred to as the inflammatory response. This response occurs in ischemia-reperfusion damage associated with stroke, various forms of neurotrauma, infectious diseases and neurodegenerative diseases such as Alzheimer s disease. Inflammation in the nervous system differs from that in other tissues. If the blood-brain barrier is broken, blood-borne inflammatory cells (e.g. polymorphonuclear leukocytes, monocytes, macrophages) invade the intercellular space and glial cells are activated, particularly microglia, which play a prominent role in the inflammatory response. These responses may... 

The manifestations of inflammation with deep-seated infections such as meningitis, pneumonia, endocarditis, and urinary tract infection must be ascertained by examining tissues or fluids. For example, the presence of polymorphonuclear leukocytes (neutrophils) in spinal fluid, lung secretions (sputum), and urine is highly suggestive of bacterial infection. 

Mechanism of Action An adrenocortical steroid that controls the rate of protein synthesis, depresses the migration of polymorphonuclear leukocytes and fibroblasts, reduces capillary permeability, and prevents or controls inflammation. Therapeutic Effect Decreases tissue response to inflammatory process. 

Mechanism of Action An adrenocortical steroid that suppresses migration of polymorphonuclear leukocytes and reverses increased capillary permeability Therapeutic Effect Decreases inflammation. 

Prostaglandins have been implicated both in the induction of inflammation and in its relief. In inflammation small blood vessels become dilated, and fluid and proteins leak into the interstitial spaces to produce the characteristic swelling (edema). Many polymorphonuclear leukocytes attracted by chemotactic factors that include LTB4309 (Chapter 19) migrate into the inflamed area, engulfing dead tissue and bacteria. In this process lysosomes of the leukocytes release phospholipase A, which hydrolyzes phospholipids and initiates the arachidonate cascade. The leukotrienes that are formed promote the inflammatory response. However, cAMP can suppress inflammation, and PGE2 has a similar effect. Indeed, E prostaglandins, when inhaled in small amounts, relieve asthma. 

Arachidonic acid released from membrane phospholipids or other sources is metabolized by the LO pathway to the smooth muscle contractile and vasoactive leukotrienes (LT), LTC4, and LTD4, as well as to the potent chemoattractant LTB4. These molecules are intimately involved in inflammation, asthma, and allergy, as well as in other multiple physiological and pathological processes. For example, cirsiliol (3, 4, 5-trihydroxy-6,7-dimethoxyflavone) proved to be a potent inhibitor of 5-LO (IC50, 0.1 pM) derived from basophilic leukemia cells and peritoneal polymorphonuclear leukocytes. 

The acute inflammatory process is associated initially with increased HA levels, the result of the cytokines released by the polymorphonuclear leukocytes, the predominant cells of the acute inflammatory process. The erythema, swelling, and warmth of the acute process are followed later by the characteristic dry appearance and the formation of wrinkles. The precise mechanisms are unknown, but may relate to the differences between acute and chronic inflammatory cells and the attendant chemical mediators released by such cells. Alternatively, initiation of a wound healing response, with collagen deposition, may be a mechanism invoked for the premature aged appearance of the skin in chronic inflammation. 

Hypophysectomy leads to an 80% decrease in interstitial fluid volume which is returned to normal by injection of hCG. The mediator of this effect is either produced directly by the Leydig cells in response to LH or originates in other cell types, e.g., macrophages or Sertoli cells in response to Leydig cell factors. The increases in interstitial fluid volume may be caused by mechanisms similar to those inducing oedema in acute inflammation. After hCG treatment, polymorphonuclear leukocytes (PMNs) accumulate in testicular blood vessels prior to the increases in the interstitial fluid volume and then migrate into the interstitial spaces 4 and 8 h after injection this invasion by PMNs may be caused by the release of a chemotactic agent [97]. 

Inflammation is a spontaneous, physiological reaction which protects the host against hostile environments and which is focussed on protection from invasion of foreign organisms and mechanical injury. Inflammation is associated with a dramatic rise in the number of polymorphonuclear leukocytes (PMNs) and monocytes in the affected tissues (e.g. articular joint space during... 

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