Anti-inflammatory responses

The glucocorticoids influence or regulate functions such as the immune response system, the regulation of glucose, fat and protein metabolism, and control of the anti-inflammatory response. Table 50-1 describes the activity of the glucocorticoids within the body. 

Nonsteroidal anti-inflammatory drugs (NSAIDs) may be initiated if acetaminophen therapy fails. At equipotent doses, all NSAIDs elicit similar analgesic and anti-inflammatory responses. Selection is based on patient preference, dosing frequency, tolerability, and cost. 

There are few clinical data regarding IL-10 in human septicemia and septic shock. Marchant et al. (M8) found high IL-10 levels in 22 of 48 patients with nor-motensive sepsis (46%) and in 17 of 21 patients with septic shock (81 %). Patients with septic shock had higher IL-10 levels, peaking during the first 48 hours and remaining detectable for 3-5 days after admission. Possibly, the intensity of the anti-inflammatory response of IL-10 is related to the importance of macrophage activation (El4). In addition, IL-10 was associated with the development of sepsis in patients with severe trauma (S19). 

Brattig, N.W., Rathjens, U., Ernst, M., Geisinger, F., Tischendorf, F.W. and Renz, A. (2000) Lipopolysaccharide-like molecules from Wolbachia endobacteria of the filaria Onchocerca volvulus are candidate mediators in the sequence of inflammatory and anti-inflammatory responses of human monocytes. Microbes and Infection2, 1—11. 

Oxazolidin-5-ones (11.110) are structurally related to oxazolidines, combining the motifs of a lactone and an O-Mannich base. These derivatives have already been discussed in Sect. 8.7.5. However, they serve here as a transition to [3,1 ]benzoxazepin-4-ones as an example of potential prodrugs. Thus, [3,l]benzoxazepin-4-one derivatives (11.111, R = H or Me, R = H, Me, Et, or Ph) were prepared from diclofenac (11.112) [137]. These prodrugs were stable for at least a few hours in simulated gastric juice, but, when administered to rats elicited an anti-inflammatory response comparable to that of diclofenac. One compound (11.111, R = Me, R = Et) was even more active than diclofenac without producing the gastric mucosal injury (ulcers) caused in all rats by diclofenac itself. Here again, there was no indication of whether the mechanism of hydrolysis is chemical or enzymatic. 

In this chapter, we will review studies on formulation variables affecting monocyte and macrophage targeting (e.g., size and number of vesicles), in vitro characterization in cell cultures, and in vivo immunomodulation and anti-inflammatory responses. 

Murray PJ. 2006. Understanding and exploiting the endogenous interleukin 10/STAT3-mediated anti-inflammatory response. Curr Opin Pharmacol. 6 379-386. 

Elkasmi KC, Holst J, Coffre M, Mielke C, et al. 2006. General nature of the STAT3-activated anti-inflammatory response. J Immunol. 177 7880-7888. 

Recently, numerous possible ways have been identified by which resveratrol may attenuate inflammation in various organs. The anti-inflammatory response of resveratrol was realized from its ability to down-regulate pro-inflammatory... 

Adverse effects of antimicrobials are treated with antihistamines (Benadryl), epinephrine (adrenalin), and steroids for anti-inflammatory response. 

Multiple-organ dysfunction syndrome (MODS) Compensatory anti-inflammatory response syndrome (CARS)... 

APACHE Acute Physiology and Chronic Health Evaluation ARDS acute respiratory distress syndrome CARS compensatory anti-inflammatory response syndrome Cl cardias index... 

Another effect of ES-62 was observed in macrophages which, after undergoing suppression of IL-12, IL-6 and TNF-a production, drive to an anti-inflammatory response (Goodridge et al. 2001). 

Ad-5 Human (Limbourg et al., 1996) Increased preadipocyte differentiation (So et al., 2005) Anti-inflammatory response determined by infection (So et al., 2005)... 

The infected group accumulated more body fat, which accounted for the increased body weight. The authors suggest that like Ad-36, increased preadipocyte differentiation by viral infection (Vangipuram et al., 2004) may be responsible for the increased body fat. Alternatively, the authors proposed the effect of inflammation on lipid metabolism. PPAR-y is a pivotal transcription factor responsible for adipocyte differentiation and is also involved in modulating inflammatory response (Clark, 2002). The authors speculated that increased adiposity may be a side effect of the anti-inflammatory response elicited by Ad-5 infection. 

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