Inflammation resolution

Schwab, J. M., Chiang, N., Arita, M., and Serhan, C. N. (2007). Resolvin El and protectin DI activate inflammation-resolution programmes. Nature 447, 869-874. 

Lu Y., Hong S., Gotlinger K., and Serhan C. N. (2006). Lipid mediator informatics and pioteomics in inflammation-resolution. The Scientific World J. 6 589-614. 

Fig. 1. Chemical mediators in inflammation resolution counterregulatory signals.

Table 1. Actions of LXs, ATL stable analogs and novel omega n-3 PUFA-derived resolvins in inflammation resolution... 

Langstrom B, Andren PE, Lindhe O, Svedbeig M, Hall H (2007) In vitro imaging techniques in neurodegenerative diseases. Mol Imaging Biol 9 161-175 Lu Y, Hong S, GotUnger K, Serhan CN (2006) Lipid mediator informatics and proteomics in inflammation-resolution. Sci World J 6 589-614... 

Hong, S., T. F. Porter et al. 2008. Resolvin El metabolome in local inactivation during inflammation-resolution. J Immunol 180(5) 3512-3519. 

Norhng, L. V., M. Spite et al. 2011. Cutting edge Humanized nano-proresolving medicines mimic inflammation-resolution and enhance wound healing. 186(10) 5543-5547. 

Primary Irritancy Studies. These studies are employed to determine the potential of materials to cause local inflammatory effects in exposed body surfaces, notably skin and eye, following acute or short-term repeated exposure. In general, the approach involves applying the test material to the surface of the skin or eye, and observing for signs of inflammation, their duration, and resolution. Reviews have been written about the conduct of primary eye irritation (58,86,87) and primary skin irritation studies (88,89). 

Inflammation occurs when a living tissue is injured or infected by microorganisms. It is a beneficial, self-limited response that requires phagocytic cells and elements of circulating plasma to enter the affected area. In principle it may achieve resolution and repair as the ideal outcome of inflammation. The persistent accumulation and activation of leukocytes is a hallmark of chronic inflammation. 

The objectives of the inflammatory response can be viewed as a hierarchical ordered panel of events. The most successful consequence of an inflammatory response is the complete restoration of function and structure of the affected tissue, also denoted as resolution. If this is not possible, inflammation aims for healing by repair and replacement of lost tissue by scar tissue. 

The key factor in the development of sepsis is inflammation. Inflammation is intended to be a local and contained response to infection or injury. Infection or injury is controlled through pro- and anti-inflammatory mediators. Pro-inflammatory mediators facilitate clearance of the injuring stimulus, promote resolution of injury, and are involved in processing of damaged tissue.1,13-16 In order to control the intensity and duration of the inflammatory response, antiinflammatory mediators are released that act to regulate pro-inflammatory mediators.15-16 The balance between pro- and anti-inflammatory mediators localizes infection/injury of host tissue.13-16 However, systemic responses ensue when equilibrium in the inflammatory process is lost. 

For infections of the skin, patients should notice relief of symptoms, including pruritus, scales, and inflammation, within 1 to 2 weeks. Therapy should be continued at least 1 week after complete resolution of symptoms. If the condition worsens or does not resolve within 4 weeks, the patient should be treated with oral therapy. 

Corticosteroids play a key role in the management of SVCS, particularly in cases of lymphoma, because these tumors inherently respond to corticosteroid therapy. They are also helpful in the setting of respiratory compromise. Corticosteroids benefit patients who are receiving radiation therapy by reducing local radiation-induced inflammation and increased intracranial pressure. Dexamethasone 4 mg intravenously or by mouth every 6 hours is a frequently used regimen. The dosage should be tapered on completion of radiation therapy or resolution of symptoms. 

Recently, the notion that the chronicity of inflammation may not actually drive the fibrogenic process has been widely appreciated (Tables 1, 2, and 3). Some propose that it is indeed the alteration of the mesenchymal cell phenotypes that disrupts the balance between collagen synthesis and degradation in the wound-healing process, highlighted by clinical evidence that shows unsuccessful treatment of fibrosis with anti-inflammatory or immunosuppressive drugs (18,19). One scenario is that mesenchymal cells (myofibroblasts and fibroblasts) are phenotypically altered and thus do not undergo apoptosis after resolution. 

Patients with acute gout should be monitored for symptomatic relief of joint pain as well as potential adverse effects and drug interactions related to drug therapy. The acute pain of an initial attack of gouty arthritis should begin to ease within about 8 hours of treatment initiation. Complete resolution of pain, erythema, and inflammation usually occurs within 48 to 72 hours. 

Goals of treatment include resolution of acute inflammatory processes, resolution of attendant complications (e.g., fistulas, abscesses), alleviation of systemic manifestations (e.g., arthritis), maintenance of remission from acute inflammation, or surgical palliation or cure. 

Bacterial sinusitis can be categorized into acute and chronic disease. Acute disease lasts less than 30 days with complete resolution of symptoms. Chronic sinusitis is defined as episodes of inflammation lasting more than 3 months with persistence of respiratory symptoms. 

High-resolution- Normal Inflammation of the Large holes in Air trapping... 

Kearley J, Barker JE, Robinson DS, Lloyd CM Resolution of airway inflammation and hyperreactivity after in vivo transfer of CD4+CD25-I- regulatory T cells is interleukin-10 dependent. J Exp Med 2005 202 1539-1547. 

T-Regulatory Cells in the Natural Resolution of Autoimmune and Allergic Inflammation... 

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