Inflammation acute/chronic

Because of its role in mediating acute/chronic inflammation, (downward) modulation of IL-1 levels may prove effective in ameliorating the clinical severity of these conditions. Again, several approaches may prove useful in this regard, including administration of ... 

Skin. The skin may become contaminated accidentally or, in some cases, materials may be deHberately appHed. Skin is a principal route of exposure in the industrial environment. Local effects that are produced include acute or chronic inflammation, allergic reactions, and neoplasia. The skin may also act as a significant route for the absorption of systemicaHy toxic materials. Eactors influencing the amount of material absorbed include the site of contamination, integrity of the skin, temperature, formulation of the material, and physicochemical characteristics, including charge, molecular weight, and hydrophilic and lipophilic characteristics. Determinants of percutaneous absorption and toxicity have been reviewed (32—35,42,43,46—49). 

Hepatitis is acute or chronic inflammation of the liver, which is frequently caused by infection with hepato-tropic viruses. Several forms of viral hepatitis (A, B, C, D, E) are known, which result from infection with viruses belonging to separate virus families, differing in their genomic organization, replication strategies, morphology and modes of transmission. 

Gastritis Acute or chronic inflammation of the lining of the stomach. 

Hughes PM, Botham MS, Frentzel S, et al. Expression of fractalkine (CX3CL1) and its receptor, CX3CR1, during acute and chronic inflammation in the rodent CNS. Glia 2002 37 314-327. 

The inflammatory response changes with time and can be divided into phases. The rapid phase occurs within seconds to minutes and consists of vasodilation, increased blood flow, edema, and pain. The acute phase is characterized by induction of inflammatory genes by NF-kB and other transcription factors. During this phase, moderate amounts of inflammatory mediators are produced. The chronic phase occurs over months to years and is marked by dramatically increased production of inflammatory mediators. The secondary chronic phase of inflammation occurs after years of oxidative damage has degraded blood vessels and tissues. Such chronic inflammation appears to play a role in many disease states, such as arteriosclerosis and cancer. 

Gastrointestinal Effects. Histological examination of stomach and intestines of rats and mice with acute- or intermediate-duration exposure to 2,3-benzofuran by gavage showed no compound-related lesions, but chronic exposure caused forestomach hyperplasia in rats and mice (NTP 1989). Male rats exposed for 103 weeks had a significant increase in chronic inflammation of the forestomach at a dose of 30 mg/kg/day, and significant increases in... 

Finally, NO has significant involvement in both acute and chronic inflammation. In acute inflammation, NO promotes swelling and increased vascular permeability. In animal models of acute inflammation, NOS inhibitors have a dose-dependent protective effect. In models of chronic inflammation (arthritis), NO is detrimental and L-arginine supplementation causes inflammatory exacerbation. At a molecular level, NO stimulates inflammation by activating the cyclooxygenase enzyme. Further supportive data are provided by the observation that fluid drained from the swollen joints of people with arthritis contains peroxynitrate and other oxidation products of NO. 

Contaminated Acute nonpurulent inflammation major technique break or major spill from hollow organ penetrating trauma less than 4 hours old chronic open wounds to be grafted or covered expected infection rate about 20%. 

In preclinical studies, a number of TCAs (imipramine, amitriptyline, nortriptyline, desipramine) were shown to inhibit pain behavior in the formalin test after systemic as well as after i.t. administration, and this effect did not seem to be related to an antiinflammatory effect of these drugs (Sawynok and Reid, 2001). The effects of TCAs in preclinical acute pain models (involving acute thermal or mechanical stimuli) have been reviewed by Eschalier et al. (1999). TCAs were also active in models of chronic inflammation (Butler et al., 1985) and in models of neuropathic pain involving nerve injury (e.g. Ardid and Guilbaud, 1992 Abdi et al., 1998). 

R12,495AA on afferent-evoked spinal synaptic transmission in vitro and on models of acute and chronic inflammation in the rat, J. Pharmacol. Exp. Ther. 2000, 294, 876-883. 

Furthermore, the immunologic pathway involved in the pathophysiology of AD is complex (table 2). It presents a degree of complexity which has not been appreciated with allergic rhinitis and asthma. In AD both Thl and Th2 T cell products play a role in chronic inflammation, which is maintained by both IL-5 (Th2) and IFN-y (Thl) [51]. In addition recent studies have demonstrated different cytokine expressions in acute (predominantly IL-16) and in chronic (mainly IL-12 and GM-CSF) lesions [52, 53]. 

The identity of factors released from damaged neurons to signal microglial cell activation may depend upon which type of neural cell is damaged, neuron versus glial, and on the the toxin or stimulus, glutamate versus /1-amyloid versus a-synuclein, and the nature of cellular death, apoptosis versus necrosis. Similarly, the molecular mechanisms and internal and external factors that modulate the dynamic aspects of acute and chronic inflammation in cell injury mediated by glutamate remain unclear. It also remains unclear to what extent inflammation is beneficial... 

Com silk possesses diuretic and stone-reducing properties. It has been used for cystitis, urethritis, nocturnal enuresis, prostatitis, and specifically for acute or chronic inflammation of the urinary system. 

Colchicine is another possible candidate for the treatment of Alzheimer s disease. This drug effectively treats familial Mediterranean fever, a condition in which recurrent inflammation and renal amyloidosis occur. Although the amyloid constituents in familial Mediterranean fever and Alzheimer s disease differ, both illnesses involve chronic inflammation, elevated acute-phase proteins, and abnormal processing of a precursor protein leading to deposition of insoluble amyloid fragments. These similarities suggest the potential therapeutic efficacy of colchicine for patients with Alzheimer s disease. 

Nitric oxide has a role in both acute and chronic inflammation. NOS-3 is involved in the vasodilation associated with acute inflammation. In experimental models of acute inflammation, inhibitors of NOS-3 have a dose-dependent protective effect, suggesting that nitric oxide promotes edema and vascular permeability. Nitric oxide has a detrimental effect in chronic models of arthritis dietary L-arginine supplementation exacerbates arthritis whereas protection is seen with NOS-2 inhibitors. Psoriasis lesions, airway epithelium in asthma, and inflammatory bowel lesions in humans all demonstrate elevated levels of nitric oxide and NOS-2. Synovial fluid from patients with arthritis contains increased oxidation products of nitric oxide, particularly peroxynitrite. 

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