Air pouch

Murphey, D. K., and Buescher, E. S. (1993). Human colostrum has anti-inflammatory activity in a rat subcutaneous air pouch model of inflammation. Pediatr. Res. 34, 208-212. 

The synthesized pyrroloquinazoline alkaloid as shown in Fig. 23 selectively inhibited COX-2 (IC5o = 1.2 pM) over COX-1 (IC50 > 10 pM) activity in human monocyte assays. In a purified ovine enzyme assay, the COX-1 activity was not affected even at a concentration over 50 pM compared to an IC50 value of 20.5 pM for COX-2 inhibition. The LOX efficacy was demonstrated by measuring LTB4 production in a mouse air pouch model [148]. 

Ford et al. (1995) assessed the intestinal permeability changes induced by non-steroidal antiinflammatory drugs in the rat. A subcutaneous air pouch was formed by injection of 10 ml sterile air prior to the experiment. Five ml of a 0.4 % carrageenan solution were injected into the pouch simultaneously with a subcutaneous injection of various doses of the non-steroidal anti-inflammatory drug and the rats allowed access to food. After various time intervals, different markers were given orally and urine collected for 5 h. The use of [51Cr]-EDTA as marker was found to be the most sensitive and reproducible method. The results correlated well with data of ulcer formation. 

Ohuchi, K., Hirasawa, N., Takeda, H., Asano, K., Watanabe, M. and Tsurufuji, S. (1987). Mechanism of antianaphylactic action of 0-agonists in allergic inflammation of air pouch type in rats. Int. Arch. Allergy Appl. Immunol. 82, 26-32. 

Sedgwick, A.D. Lees, P. (1986) Studies of eicosanoid production in the air pouch model of synovial inflammation. Agents and Actions, 18, 429-438. 

The intraperitoneal administration of berbamine into rats suppressed subcutaneous rat air pouch leukocyte infiltration that was induced by interleukin-1 (1L-1), tumor necrosis factor (TNF), and platelet-activating factor (PAF), at an EDJ0 20-30 mg/kg/3 days. The utilization of berbamine may be of value in the therapy of chronic inflammatory diseases where IL-1, TNF, and PAF play in role in pathogenesis [177]. 

Angiogenesis Prophylactic treatment with ATL-1 protected against angiogenesis and CD-31 expression in a murine air pouch model of angiogenesis ATL-1 potently inhibits endothelial cell proliferation ATL-1 inhibits VEGF-induced endothelial cell chemotaxis Fierro et al 2002 Fierro et al 2003... 

The anti-inflammatory effects of borage seed oil have been demonstrated in animal models. A diet enriched with borage seed oil (23% GLA) was compared to one with safflower oil (<1% GLA) with regard to effects on acute inflammation induced by monosodium urate crystals, subacute or chronic inflammation caused by Freund s adjuvant in a subcutaneous air pouch, or adjuvant-induced arthritis (Tate et al., 1989). Borage seed oil, but not safflower oil, decreased inflammation in all models. In addition, the ratio of DGLA to AA was five times that in the livers of animals fed safflower oil. 

Its mechanism of action, however, is not completely elucidated. Kamakura et al. [94] studied the effects of stem bromelain on the plasma kallikrein system, bradykinin levels and plasma exudation at the inflammatory site in rats with a kaolin-induced inflammation of an air pouch. Bromelain caused a dose-dependent decrease of bradykinin levels (measured with the method of Minami et al. [95]) at the inflammatory site and a parallel decrease of the prekallikrein levels in sera [88]. Plasma exudation was also reduced dose-dependently. Bradykinin-degrading activity in sera was elevated after bromelain treatment, but not in the pouch fluid. The authors conclude that bromelain inhibits plasma exudation through inhibition of the bradykinin generation at the inflammatory site via depletion of the plasma kallikrein system. Bromelain also shows a dose-dependent analgesic effect in concanavalin A-injected paws of 5.6 mg/kg i.v.), considered to be due to decrease of high molecular weight kininogen [96]. 

Stevens, A.J. Martin, S.W. Brennan, B.S. McLachlan, A. Gifford, L.A. Rowland, M. Houston, J.B. Regional drug delivery II Relationship between drug targeting index and pharmacokinetic parameters for three non-steroidal anti-inflammatory drugs using the rat air pouch model of inflammation. Pharm.Res., 1995, 12, 1987-1996... 

Table 5. The ID50 Values of Neolignans and Hydrocortisone for Inhibition of Angiogenesis and Granuloma Formation in Mouse Air Pouch...

Caffeic Acid Phenethyl Ester (CAPE). CAPE, a phenolic compound with antioxidant properties, is an active ingredient derived from honeybee propolis (52). CAPE has antiviral, anti-inflammatory and antiproliferative properties. The compound differentially suppresses the growth of numerous human cancer cells and also inhibits tumor promoter-mediated processes in transformed cells (53,54). In transformed cells, CAPE induces apoptosis and inhibits the expression of the malignant phenotype (55,56). In addition, CAPE treatment attenuates the formation of azoxymethane-induced aberrant crypts and the activities of ornithine decarboxylase (ODC), tyrosin protein kinase, and lipoxygenase activity (57). Although the molecular basis for these multiple chemopreventive effects of CAPE is not clear, recent studies have demonstrated that CAPE is a potent and specific inhibitor of the transcription factor NF-kB (58). CAPE inhibited the activity and expression of COX-2 in the carrageenan air pouch model of inflammation as well as in TPA-treated human oral epithelial cells (59). CAPE was able to reduce neointimal formation by inhibiting NF-kB activation in a model of endothelial injury of rat carotid artery (60). 

Specific antibodies. This is a very important aspect as there are many examples of chemokines that do not have cross-species function. Different compartments in mice may be used to investigate the recruitment of leukocytes after injection of a chemokine, including the peritoneum, pleura, joints, and air pouch cavities. The choice of the cavity must be careful as it is influenced by its size (accuracy to inject the chemokine), the basal levels of resident cells (interference in the readout of recruited cells), the option of a technique to identify the cell population (low or high number of recruited cells), and the possibility that a functional readout may be obtained (for instance, the capacity to induce pain when the chemokine is injected in the joint). 

The generation of an air pouch in mice allows us to easily study in vivo the inflammatory response to chemokines by retrieving the infiltrating inflammatory cells. 20—30 g female BALB/c mice (around 8—10 weeks old) should be used to perform these experiments, because, in heavier mice, it is more difficult to correctly form the air pouch (AH et al., 2005). This study has been written with chemokine as the Hgand, but it is vahd for any chemoattractant. 

Figure 5 Schematic of the murine air-pouch in vivo chemotaxis model. BALB/c mice were anesthetized, their backs were shaved, and the shaved sites were injected with 3 ml of sterile air under the skin. This was repeated on days 2, 4, and 5, and 1 ml of air was injected to create the air pouch.

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