Inhibition of pulmonary eosinophilia and airway hyperresponsiveness in allergic mice by rolipram: involvement of endogenously released corticosterone and catecholamines

Kung, Ted T.; Crawley, Yvette; Luo, Bin; Young, Simon S.; Kreutner, William; Chapman, Richard W.

doi:10.1038/sj.bjp.0703308

Cited by 33 publications

(17 citation statements)

References 27 publications

(45 reference statements)

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“…These results were supported by findings from previous studies, in which inhibition of PDE-4 caused an increase in plasma corticosterone levels in rats (Kumari et al, 1997;Kung et al, 2000;Jabaris et al, 2015). Contrasting reports from previous studies demonstrated that exogenous administration of corticosterone and elevation of the hormone in circulation following stress exposure reduced hippocampal synaptic potentiation and hippocampus-specific learning and memory (Kim et al, 2001;Alfarez et al, 2002;Woodson et al, 2003).…”

Section: Discussioncontrasting

confidence: 77%

Phosphodiesterase-4 inhibitors ameliorates cognitive deficits in deoxycorticosterone acetate induced hypertensive rats via cAMP/CREB signaling system

Sumathy

Girish

et al. 2015

Brain Research

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Section: Discussioncontrasting

confidence: 77%

Phosphodiesterase-4 inhibitors ameliorates cognitive deficits in deoxycorticosterone acetate induced hypertensive rats via cAMP/CREB signaling system

Sumathy

Girish

et al. 2015

Brain Research

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“…In one study, the inhibitory effect of rolipram on TNF-␣ induction during streptococcal cell wall-induced arthritis was reversed by the GR antagonist, RU486 (Laemont et al 1999). In another study, the glucocorticoid synthesis inhibitor, metyrapone, was found to attenuate rolipram-induced inhibition of pulmonary eosinophilia in allergic mice (Kung et al 2000). Complementing these studies are a number of reports demonstrating comparable immunologic effects of glucocorticoids and rolipram on cytokine induction (decreased TNF-␣ and increased interleukin (IL)-10 and IL-4) as well as inflammation (e.g.…”

Section: Discussionmentioning

confidence: 97%

“…Finally, rolipram does not appear to A number of studies have documented the wideranging effects of rolipram on cellular activity in both the immune system and the brain. Immunologic studies have shown that rolipram has potent antiinflammatory effects, exhibiting inhibition of the proinflammatory cytokine, TNF-␣, and providing protection from several autoimmune disorders (Ross et al 1997;Laemont et al 1999;Kung et al 2000;Knox 2000, 2001;Sekut et al 1995;Eigler et al 1998;Sommer et al 1997). Indeed, it has been suggested that rolipram may serve as an effective therapy for human autoimmune disorders, including multiple sclerosis (Sommer et al 1997).…”

Section: Discussionmentioning

confidence: 99%

The Phosphodiesterase Type 4 Inhibitor, Rolipram, Enhances Glucocorticoid Receptor Function

Miller

Vogt

Pearce

2002

Neuropsychopharmacology

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Previous studies have demonstrated that antidepressants can enhance glucocorticoid receptor (GR) translocation and function, possibly through activation of cAMP and downstream cAMP dependent protein kinases. Accordingly, we examined GR function in cells treated with rolipram, a phosphodiesterase (PDE) type 4 inhibitor that antagonizes cAMP breakdown. Compared with vehicle-treated cells, rolipram alone and in combination with dexamethasone significantly enhanced GR function as measured in both mouseHyperactivity of the hypothalamic-pituitary adrenal (HPA) axis is a common and reproducible finding in patients with major depression (Pariante and Miller 2001;Holsboer 2000). A major factor responsible for these HPA axis changes is believed to be increased corticotropin releasing hormone (CRH), which may also contribute to the behavioral features of this disorder (Owens and Nemeroff 1993). Altered feedback regulation of CRH by glucocorticoids is one mechanism that may contribute to the CRH changes found in major depression (Pariante and Miller 2001;Holsboer 2000). Specifically, evidence exists that the receptors for glucocorticoids may become impaired in major depression, leading to glucocorticoid resistance in selected body tissues including the brain and immune system (Pariante and Miller 2001;Holsboer 2000). Recent evidence suggests that antidepressants may reverse glucocorticoid receptor changes in depression by direct effects on the glucocorticoid receptor (GR) (Pariante and Miller 2001;Holsboer 2000;Holsboer and Barden 1996). Both in vitro and in vivo data indicate that antidepressants can increase GR number and facilitate GR function (Pariante and Miller 2001;Holsboer and Barden 1996). Given evidence that a number of antidepressants have effects on signal transduction pathways involving cyclic AMP NO . 6 (cAMP) (Chen and Rasenick 1995a,b;Nestler et al. 1989;Nibuya et al. 1996), there has been speculation that the influence of antidepressants on GR is through their effects on cAMP-related signal transduction events (Pariante and Miller 2001).A large body of data demonstrates that cAMP signal transduction pathways are involved in the regulation of the GR. For example, direct evidence of facilitation of GR function has been demonstrated for ␤ 2 receptor agonists, cAMP, and protein kinase A (PKA) (Eickelberg et al. 1999;Schmidt et al. 2001;Sato et al. 1996;Rangarajan et al. 1992). Phosphodiesterases (PDE) are a group of enzymes that catalyze the breakdown of cyclic nucleotides (Beavo et al. 1994). The PDE isozyme type 4 is specific for cAMP and is expressed throughout the brain and immune system (Perez-Torres et al. 2000;Engels et al. 1994). Thus, inhibitors of PDE type 4 provide a pharmacologic strategy to increase prevailing cAMP levels in relevant target tissues.One PDE type 4 inhibitor, rolipram, has been shown to have antidepressant effects (Zhu et al. 2001;Bobon et al. 1988, Eckmann et al. 1988. Rolipram was first demonstrated to have potent antidepressant activity in animal models (Zhu et al. 2001;Wachte...

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“…Mice were then tested for airway hyperresponsiveness to metacholine by the forced oscillation technique as previously described (21). A Student's t test was used to determine statistical significance between groups, with p Ͻ 0.5 being considered significant.…”

Section: Airway Hyperreactivitymentioning

confidence: 99%

New IL-17 Family Members Promote Th1 or Th2 Responses in the Lung: In Vivo Function of the Novel Cytokine IL-25

Hurst

Muchamuel

Gorman

et al. 2002

The Journal of Immunology

566

512

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We have biologically characterized two new members of the IL-17 cytokine family: IL-17F and IL-25. In contrast to conventional in vitro screening approaches, we have characterized the activity of these new molecules by direct in vivo analysis and have compared their function to that of other IL-17 family members. Intranasal administration of adenovirus expressing IL-17, IL-17C, or IL-17F resulted in bronchoalveolar lavage neutrophilia and inflammatory gene expression in the lung. In contrast, intranasal administration of IL-25-expressing adenovirus or IL-25 protein resulted in the production of IL-4, IL-5, IL-13, and eotaxin mRNA in the lung and marked eosinophilia in the bronchoalveolar lavage and lung tissue. Mice given intranasal IL-25 also developed epithelial cell hyperplasia, increased mucus secretion, and airway hyperreactivity. IL-25 gene expression was detected following Aspergillus and Nippostrongylus infection in the lung and gut, respectively. IL-25-induced eosinophilia required IL-5 and IL-13, but not IL-4 or T cells. Following IL-25 administration, the IL-5+ staining cells were CD45R/B220+, Thy-1+/−, but were NK1.1-, Ly-6G(GR-1)-, CD4-, CD3-, and c-kit-negative. γ-common knockout mice did not develop eosinophilia in response to IL-25, nor were IL-5+ cells detected. These findings suggest the existence of a previously unrecognized cell population that may initiate Th2-like responses by responding to IL-25 in vivo. Further, these data demonstrate the heterogeneity of function within the IL-17 cytokine family and suggest that IL-25 may be an important mediator of allergic disease via production of IL-4, IL-5, IL-13, and eotaxin.

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Inhibition of pulmonary eosinophilia and airway hyperresponsiveness in allergic mice by rolipram: involvement of endogenously released corticosterone and catecholamines

Cited by 33 publications

References 27 publications

Phosphodiesterase-4 inhibitors ameliorates cognitive deficits in deoxycorticosterone acetate induced hypertensive rats via cAMP/CREB signaling system

Phosphodiesterase-4 inhibitors ameliorates cognitive deficits in deoxycorticosterone acetate induced hypertensive rats via cAMP/CREB signaling system

The Phosphodiesterase Type 4 Inhibitor, Rolipram, Enhances Glucocorticoid Receptor Function

New IL-17 Family Members Promote Th1 or Th2 Responses in the Lung: In Vivo Function of the Novel Cytokine IL-25

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