Differential effects of indomethacin and dexamethasone on cytokine production in carrageenin-induced rat pleurisy

Utsunomiya, Iku; Nagai, Susumu; Oh‐ishi, Sachiko

doi:10.1016/0014-2999(94)90599-1

Cited by 55 publications

(28 citation statements)

References 24 publications

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“…This feature was very different from the case of carrageenin-induced pleurisy in rats. In fact, several investigators, including us, reported that leukocyte migration was suppressed by indomethacin in rat pleurisy (Vannier et al, 1988;Utsunomiya et al, 1994;Ogino et al, 1996). Although the difference in prostanoid involvement in leukocyte migration between mice and rats suggests different regulation of chemokine or cytokine induction by the prostanoids, the precise mechanism leading to leukocyte migration remains to be determined.…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin Receptors EP2, EP3, and IP Mediate Exudate Formation in Carrageenin-Induced Mouse Pleurisy

Yuhki¹,

Ueno²,

Naraba³

et al. 2004

J Pharmacol Exp Ther

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The roles of prostaglandins (PGs) as mediators of inflammation have been extensively studied, and production of PGI 2 and PGE 2 at inflammatory sites has been reported. However, it has not yet been clarified which type of PG receptors has a major role in inflammatory exudation. To examine in vivo role of PG receptors in inflammatory exudation, we induced pleurisy in PG receptors (IP, EP1, EP2, EP3, or EP4) knockout mice by intrapleural injection of carrageenin. Pleural exudate accumulation in wild-type (WT) mice at 1 to 5 h, but not at 24 h, was significantly attenuated by the pretreatment with indomethacin, indicating that PGs are responsible for exudate formation at the early phase of pleurisy. Pleural exudation at 1 to 5 h in IP, EP2, or EP3 knockout mice, but not in EP1 and EP4 knockout, was significantly reduced compared with in WT mice. In the exudates, 6-keto-PGF 1 ␣ and PGE 2 were detected as the major PGs, each with its peak concentration at 3 h. In addition, involvement of bradykinin in the phenomenon was suggested by the fact that captopril, a kininase inhibitor, enhanced the exudate formation and increased the amount of 6-keto-PGF 1 ␣ and PGE 2 and that a bradykinin B2-receptor antagonist inhibited the exudate formation. In contrast, leukocyte migration into pleural cavity was not influenced by indomethacin-treatment nor by these receptor deficiencies. These results demonstrate participation of EP2 and EP3 along with IP in pleural exudate formation but not in leukocyte migration in carrageenin-induced mouse pleurisy.

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Section: Discussionmentioning

confidence: 99%

Prostaglandin Receptors EP2, EP3, and IP Mediate Exudate Formation in Carrageenin-Induced Mouse Pleurisy

Yuhki¹,

Ueno²,

Naraba³

et al. 2004

J Pharmacol Exp Ther

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“…In addition to infiltrating cells, mesothelial cells actively participate in pleuralinflammation via release of various mediators and proteins [1]. Corticosteroids suppress local production of tumour necrosis factor-α, interleukin-1 and interleukin-6, cytokines that play a major role in pleural exudation and chemotaxis [2]. …”

Section: Discussionmentioning

confidence: 99%

Immunosuppressant-Responsive Idiopathic Lymphocytic Pleuritis

et al. 2005

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Lymphocyte-dominant pleural inflammation is seen in tuberculous, malignant and immune-mediated pleural disease. We describe two male patients who presented with chest pain and dyspnoea, in whom radiological and histological investigations showed idiopathic lymphocytic pleuritis that responded to immunosuppressive therapy with corticosteroids and/or azathioprine. Corticosteroid-responsive pleuritis has been described in association with many conditions, but little is known of idiopathic lymphocytic pleuritis. The authors suggest that patients with idiopathic pleural thickening undergo early thoracoscopic pleural biopsy, and that immunosuppressant therapy be considered for patients with idiopathic lymphocytic pleuritis.

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“…PMNs moving out of the circulation into the inflamed tissue have a key function in the breakdown and remodeling of injured tissue (24,25). Moreover, macrophages participate in the progression of experimental pleurisy producing proinflammatory cytokines such as TNF-␣ and IL-1␤ (26).…”

Section: T He Glucocorticoid-induced Tnfr-related Gene (Gitr)mentioning

confidence: 99%

Proinflammatory Role of Glucocorticoid-Induced TNF Receptor-Related Gene in Acute Lung Inflammation

Cuzzocrea

Nocentini

Paola

et al. 2006

The Journal of Immunology

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Glucocorticoid-induced TNFR-related gene (GITR) participates in the immune/inflammatory response. Because GITR expression has been described in cells other than T lymphocytes, we investigated whether it also modulates acute inflammatory response. Using GITR-deficient (GITR−/−) mice, we analyzed the role of GITR in the development of carrageenan-induced lung inflammation (pleurisy) by studying several proinflammatory markers 2–8 h after carrageenan injection. When compared with GITR+/+, GITR−/− mice exhibited decreased production of turbid exudate containing a lower number of leukocytes. This was correlated with the reduction of inflammatory markers (including TNF-α, IL-1β, myeloperoxidase, inducible NO synthase, and cyclooxygenase 2) in the pleural exudate and/or in the lung. Moreover, endothelial cells expressed lower levels of adhesion molecules. In lungs of GITR+/+ mice, GITR ligand expression was not modulated during pleurisy, while that of GITR increased, as a consequence of increased infiltration by GITR-expressing cells and of GITR up-regulation in macrophages and endothelial cells. Finally, cotreatment of GITR+/+ mice with carrageenan and Fc-GITR fusion protein decreased the number of inflammatory cells (pleural macrophages and lung neutrophils) as compared with carrageenan treatment alone, confirming that GITR plays a role in the modulation of pleurisy.

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Differential effects of indomethacin and dexamethasone on cytokine production in carrageenin-induced rat pleurisy

Cited by 55 publications

References 24 publications

Prostaglandin Receptors EP2, EP3, and IP Mediate Exudate Formation in Carrageenin-Induced Mouse Pleurisy

Prostaglandin Receptors EP2, EP3, and IP Mediate Exudate Formation in Carrageenin-Induced Mouse Pleurisy

Immunosuppressant-Responsive Idiopathic Lymphocytic Pleuritis

Proinflammatory Role of Glucocorticoid-Induced TNF Receptor-Related Gene in Acute Lung Inflammation

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