Effects of sera and exudate from carrageenan-treated rats on two models of acute inflammation

Sedgwick, A. D.; Koh, M. S.; Willoughby, D. A.; Pelletier, Monique

doi:10.1007/bf02004709

Cited by 18 publications

(13 citation statements)

References 16 publications

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“…The second option is introduction of sterile air into the subcutis to initiate a pouch granuloma [67], the wall of which exhibits many similarities to synovium [68, 69]. Subsequent injection of such molecules as carrageenan [70], γ -globulin [71], streptococcal cell wall fragments [72], or zymosan [73] incites an inflammatory response in the pouch that morphologically resembles acute and chronic synovitis [44]. Both xenografts and air pouches can be employed to evaluate the efficacy of therapeutic agents on synovitis and cartilage degeneration [73, 74].…”

Section: Objective 1: Available Rodent Models Of Immune-mediated Amentioning

confidence: 99%

Rodent Preclinical Models for Developing Novel Antiarthritic Molecules: Comparative Biology and Preferred Methods for Evaluating Efficacy

Bolon

Stolina

King

et al. 2010

BioMed Research International

102

121

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Rodent models of immune-mediated arthritis (RMIA) are the conventional approach to evaluating mechanisms of inflammatory joint disease and the comparative efficacy of antiarthritic agents. Rat adjuvant-induced (AIA), collagen-induced (CIA), and streptococcal cell wall-induced (SCW) arthritides are preferred models of the joint pathology that occurs in human rheumatoid arthritis (RA). Lesions of AIA are most severe and consistent; structural and immunological changes of CIA best resemble RA. Lesion extent and severity in RMIA depends on experimental methodology (inciting agent, adjuvant, etc.) and individual physiologic parameters (age, genetics, hormonal status, etc.). The effectiveness of antiarthritic molecules varies with the agent, therapeutic regimen, and choice of RMIA. All RMIA are driven by overactivity of proinflammatory pathways, but the dominant molecules differ among the models. Hence, as with the human clinical experience, the efficacy of various antiarthritic molecules differs among RMIA, especially when the agent is a specific cytokine inhibitor.

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Section: Objective 1: Available Rodent Models Of Immune-mediated Amentioning

confidence: 99%

Rodent Preclinical Models for Developing Novel Antiarthritic Molecules: Comparative Biology and Preferred Methods for Evaluating Efficacy

Bolon

Stolina

King

et al. 2010

BioMed Research International

102

121

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“…Chronic granulomas have been produced by injecting potent irritants into newly formed, i.e. 24 hours old, air pouches [2][3][4][5][22][23]. Interesting general information about mechanisms of chronic inflammation can be obtained using such pouches but they bear little resemblance to the synovial cavity.…”

Section: Hagg-indueed Inflammationmentioning

confidence: 99%

The subcutaneous air pouch model of synovium and the inflammatory response to heat aggregated gammaglobulin

et al. 1986

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Subcutaneous injection of sterile air in rodents results in the formation of an air pouch with a lining morphologically similar to synovium (Edwards et al., 1981). We extended the comparison between pouch and synovial tissue and confirmed broad similarities in structure and function but also noted important differences. The air pouch was used to study the time course of the acute inflammatory response to heat aggregated human IgG. Saline washout of the pouch allowed simultaneous measurement of cellular and mediator components of the inflammatory exudate. The aggregates were rapidly phagocytosed by the pouch lining cells, resulting in acute inflammation characterised by polymorphonuclear leucocyte infiltration with peak numbers in the exudate at 12 hours, temporally dissociated from the earlier peak of PGE2 at 3 hours.

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“…7 The air-pouch model in rodents has been extensively used to study the inflammatory granulomatous reaction characterized by a marked production of biochemical mediators in the fluid exudate as well as an influx of polymorphonuclear leucocyte (PMN) cells and macrophages. 8 PGs are one of the mediators that could be detected in the air-pouch fluid following injection of an inflammagen primarily by the induction of COX-2. 9 In the present study we have characterized the latex-induced inflammation in the rat air-pouch model and evaluated the role of COX-2 using pharmacological reagents.…”

Section: Introductionmentioning

confidence: 99%

Involvement of prostaglandins in inflammation induced by latex of Calotropis procera

Kumar

Shivkar²

2004

Mediators of Inflammation

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INTRODUCTION:The aerial parts of the plant Calotropis procera produce milky white latex that causes inflammation of the skin and mucous membranes. Prostaglandins are one of the mediators released in an inflammatory response following induction of cyclooxygenase (COX). In the present study, we have evaluated the role of prostaglandins in inflammatory response elicited by the latex of C. procera. METHODS: Aqueous extract of dried latex of C. procera was injected into the 6-day air-pouch in the rat. The inflammatory response was evaluated by studying the air-pouch fluid for its volume, protein and prostaglandin (PG) E2 concentrations, and leucocyte counts. The granulation tissue from the pouch was quantified and studied for COX-2 expression by reverse transcriptase-polymerase chain reaction. The inhibitory effect of celecoxib and dexamethasone was evaluated on the aforementioned parameters. RESULTS: Dried latex produced an inflammatory response that was maximum at 6 h. It was associated with the accumulation of protein-rich fluid, leucocytes and PGE2 production. It also resulted in granulation of the pouch cavity that was a maximum on day 3. COX-2 expression could be detected in the granulation tissue on day 1 and it increased progressively up to day 5. The anti-inflammatory drugs celecoxib and dexamethasone significantly attenuated the inflammatory response and inhibited COX-2 expression in granulation tissue. CONCLUSIONS: Latex of C. procera induces an inflammatory response characterized by an early exudative phase accompanied by PGE2 production and a late proliferative phase associated with COX-2 induction. Both the phases were effectively inhibited by COX-2 inhibitors.

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Effects of sera and exudate from carrageenan-treated rats on two models of acute inflammation

Cited by 18 publications

References 16 publications

Rodent Preclinical Models for Developing Novel Antiarthritic Molecules: Comparative Biology and Preferred Methods for Evaluating Efficacy

Rodent Preclinical Models for Developing Novel Antiarthritic Molecules: Comparative Biology and Preferred Methods for Evaluating Efficacy

The subcutaneous air pouch model of synovium and the inflammatory response to heat aggregated gammaglobulin

Involvement of prostaglandins in inflammation induced by latex of Calotropis procera

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