Prostaglandins E2, F2α, 6-keto-F1α and thromboxane B2 levels in carrageenin-induced inflammatory exudates in the rat air-pouch granuloma

doi:10.1016/0161-4630(79)90063-6

Prostaglandins and Medicine

Volume 2, Issue 4, April 1979, Pages 293-297

Prostaglandins and M...

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Abstract

Levels of PGE₂, PGF_2α, PGI₂ (measured as 6-keto-PGF_1α), and thromboxane B₂ were determined in rat inflammatory exudates induced 1, 3, and 7 days after carrageenin injection into air-pouch granuloma. The PGE₂ and 6-keto-PGF_1α levels found in the exudate could not account for the differences in PGE₂-like activity as measured by biologic and serologic methods.

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Cited by (17)

Patterns of prostaglandin E<inf>2</inf> and leukotriene B<inf>4</inf> production in inflammation induced by peptidoglycan-polysaccharide polymers of bacterial cell walls
1995, Comparative Immunology, Microbiology and Infectious Diseases
The changing levels of prostaglandin E₂ (PGE₂) and leukotriene B₄ (LTB₄) were compared over a period of 1 h to 15 days in two kinds of inflammatory responses induced in the rat air pouch by chemically similar polymers of peptidoglycan-polysaccharide (PG-PS) isolated from cell walls of group A streptococci. The smaller polymers (100 s, average mol. wt 5.3 × 10⁶) induced a more severe acute response over the first 24 h, whereas, from 3 to 15 days the larger polymers (10 p, average mol. wt 5 × 10⁸) induced greater chronic inflammation, as measured by pouch fluid volume, number of infiltrating cells and weight of granulation tissue. The most prominent difference between the two kinds of responses in the pattern of PGE₂ and LTB₄ were: (a) A shift between 1 to 6 h to much higher production of PGE₂ in the exudate induced by large polymers. During this time the level of LTB₄ also increased, but continued to be higher in the exudate induced by small polymers. (b) The sustained production of relatively high levels of LTB₄ and PGE₂ in the large polymer exudate at 15 days. Changes such as these indicate that this model is useful for analyzing mediators which regulate the evolution of acute into chronic inflammation.
Les modifications des taux de prostaglandines E₂ (PGE₂) et de leukotriènes B₄ (LTB₄) sont comparées sur une période d'une heure à 15 jours dans deux types de réponses inflammatories induites dans un sac aérien modélisé de rat par des polymères chimiquement similaires au peptidoglycan-polysaccharide (PG-PS) isolés de cellules de paroi de Streptocoques du group A. Les polymères les plus petits (100 s, PM moyen 5, 3 × 10⁶) induiraient une réponse aigüe plus sévère au delà des 24 premières heures, tandis que de 3 à 15 jours, les polymères les plus grands (10 p, PM moyen 5 × 10⁸) induiraient une inflammation chronique plus grande, aussi bien mesurée dans le volume de fluide du sac que par le nombre de cellules infiltrantes et le poids du tissu de granulation. La différence la plus importante entre les deux sortes de réponses dans l'exemple de PGE₂ et de LTB₄ était (a) un décalage d'une à 6 heures dans la plus grande production de PGE₂ dans l'exsudat induit par des polymères plus grands. Pendant ce temps, le niveau de LTB₄ a aussi augmenté mais continuait d'être plus élevé dans l'exsudat induit par les petits polymères. (b) La production soutenue de taux relativement élevés de LTB₄ et PGE₂ dans le cas des grands polymères a été excrétée à 15 jours. Des modifications telles que celles-ci indiquent que ce modèle est utile pour analyser les médiateurs qui régulent l'évolution de la phase aigüe lors d'inflammations chroniques.
The six-day-old rat air pouch model of inflammation: Characterization of the inflammatory response to carrageenan
1994, Journal of Pharmacological and Toxicological Methods
Inflammation was induced in the 6-day-old rat air pouch by injection of carrageenan. The model was characterized in terms of exudate volume, leucocyte influx, cell free protein, prostaglandin E₂ levels, and granuloma formation. The time course of all these inflammatory markers, except prostaglandin E₂, showed a 3-hr lag followed by a rapid increase to 8 hr. Thereafter, the rate of increase was much slower to 48 hr. Differential cell counts indicated a predominantly polymorphonuclear cell response (75%) during the first 48 hr. Prostaglandin E₂ levels increased rapidly after a 3-hr lag, to a maximum of 440 ± 140 ng/mL at 15 hr and thereafter quickly declined to 140 ±60 ng/mL at 21 hr. Prostaglandin E₂ levels were the most sensitive inflammatory marker to (S+)-ibuprofen and were reduced dose dependently in the range 0.05 to 1 mg/kg. We have demonstrated the time course for duration of NSAID-induced reduction of prostaglandin E₂ levels during inflammation in an individual animal. Rac-ibuprofen (0.1–1 mg/kg) reduced leucocyte influx at 3 and 5 hr, after which drug effects gradually diminished by 24 hr. Rac-ibuprofen at 1 mg/kg significantly reduced the volume of air pouch exudate recovered at 24 hr but had no effect on protein levels.
The role of eicosanoids in inflammation
1986, Progress in Lipid Research
Activation of suppressor cells by low molecular weight factors secreted by spleen cells of tumor-bearing mice: Modulatory role of prostaglandins
1986, International Journal of Immunopharmacology
We have shown previously that the spleens of mice bearing large M-1 fibrosarcomas contain inducer cells which secrete dialysable factors which activate suppressor T cells from unprimed, normal precursor spleen cells. Once activated, the suppressor cells inhibit the in vitro antibody synthesis of co-cultured syngeneic splenocytes stimulated by T cell dependent antigens. In this paper we have examined the possibility that prostaglandins are involved in the activation process. Inducer and precursor cells were cultured in Marbrook vessels in chambers separated by dialysis membranes. Using this procedure, suppressor cells were activated following 12 h of culture but were not detectable after 6 h. The cyclooxygenase inhibitors, indomethacin, acetyl salicylic acid (ASA), and ibuprofen all prevented the activation of suppressor cells in a dose dependent manner. Prostaglandin (PG) E₁, but not PGF_2α or PGD₂, restored the activation of suppressor cells in cultures containing the cyclooxygenase inhibitors. Restoration of suppressor cell activation was seen with 1 × 10⁻⁷ M PGE₁ but no activation of suppressor cells was seen in control cultures containing up to 1 × 10⁻⁵ M PGE₁. In addition, cultured spleen cells from tumor-bearing mice did not secrete higher quantities of PGE than did cells from age and sex matched normal mice. These data suggest that PGE has a modulatory rather than a direct role in the activation of suppressor cells by inducer factors from tumor-activated inducer cells.
Increasing membrane polyunsaturated fatty-acid content augments cyclic AMP formation and prostaglandin production in NIE-115 neuroblastoma
1984, Progress in Neuropsychopharmacology and Biological Psychiatry
1. Addition of linoleic acid (50 μM) to culture medium significantly increases levels of polyunsaturated fatty acids (PUFA) in membrane phospholipids of NIE-115 neuroblastoma.
2. Basal levels of cyclic AMP are elevated significantly in supplemented ceils.
3. Exogenous prostaglandins (PG) PGE₁ and PGD₂ stimulate cAMP formation in NIE-115 neuroblastoma.
4. Supplemented cells produce higher levels of PGE and PGD than do control cultures.
5. Inclusion of cyclooxygenase inhibitors in culture medium does not block elevation of cyclic nucleotide in supplemented cells.
6. Endogenous PG production and receptor activation cannot account for increased cAMP in EFA-supplemented neuroblastoma.
Phospholipase A<inf>2</inf> activity in carrageenin-induced inflammatory tissue of rats
1982, Biochemical Pharmacology
Phospholipase A₂ activity was detected in 7-day-old carrageenin-induced inflammatory tissue of rats using a synthetic substrate, 1-acyl-2-[³H]arachidonyl-phosphatidylcholine. The inflammatory tissue was homogenized in saline containing 1 M KC1, and the 105,000 g supernatant fraction was placed on a Sephadex G-100 column. The partially purified phospholipase A₂ had a pH optimum at 6–7 and was Ca²⁺ dependent. p-Bromophenacyl bromide was strongly inhibitory to the partially purified phospholipase A₂ (ic₅₀ = 1.44 × 10⁻⁵ M). A moderate inhibition was observed with indomethacin. Cycloheximide and dexamethasone, which inhibit prostaglandin production in inflammatory tissue, exerted no direct inhibitory action on the phospholipase A₂. There were no direct inhibitory effects of quinacrine, bradykinin, or actinomycin D. The cell-free supernatant fraction of the inflammatory exudate of 7-day-old carrageenin-induced granulation tissue was found to have no phospholipase A₂ activity.

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^∗: Present address: Department of Biochemistry, Faculty of Pharmaceutical Sciences, Tohoku University.

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Prostaglandins E2, F2α, 6-keto-F1α and thromboxane B2 levels in carrageenin-induced inflammatory exudates in the rat air-pouch granuloma

Abstract

Pharmacol. Res. Commun.

Biochem. Biophys. Acta

Prostaglandins

Prostaglandins

Biochem. Biophys. Res. Commun.

Prostaglandins

Biochem. Pharmacol.

Jap. J. Pharmacol.

Prostaglandins E₂, F_2α, 6-keto-F_1α and thromboxane B₂ levels in carrageenin-induced inflammatory exudates in the rat air-pouch granuloma