Modulation of Thl- and Th2-like cytokine production from mitogen-stimulated human peripheral blood mononuclear cells by phosphodiesterase inhibitors

Yoshimura, Tomoaki; Nagao, Tomomi; Nakao, Tomohiro; Watanabe, Shino; Usami, Eiseki; Kobayashi, J; Yamazaki, Futoshi; Tanaka, Hiroyuki; Inagaki, Nobuya; Nagai, Hiroichi

doi:10.1016/s0306-3623(97)00103-1

Cited by 23 publications

(13 citation statements)

References 22 publications

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“…Under Th2-promoting culture conditions, naïve T cells exposed to NE or terbutaline develop into Th2 cells, but adrenergic agents have no affect on IL-4, IL-5 or IL-10 production [139][140][141]. Other studies support a dichotomy in β 2 -AR effects on Th1 and Th2 cells, such that their activation modulates Th1 cell differentiation and cytokine production, but does not alter Th2 effector cells [131,197,203,198,[207][208][209]. Interestingly, increasing intracellular cAMP levels in Th2 cells can modulate IL-4 production [210][211][212][213].…”

Section: Functional Significance Of Sympathetic Innervation Of Secondmentioning

confidence: 99%

Sympathetic modulation of immunity: Relevance to disease

Bellinger

Millar

Perez

et al. 2008

Cellular Immunology

226

185

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Optimal host defense against pathogens requires cross-talk between the nervous and immune systems. This paper reviews sympathetic-immune interaction, one major communication pathway, and its importance for health and disease. Sympathetic innervation of primary and secondary immune organs is described, as well as evidence for neurotransmission with cells of the immune system as targets. Most research thus far as focused on neural-immune modulation in secondary lymphoid organs, and have revealed complex sympathetic modulation resulting in both potentiation and inhibition of immune functions. SNS-immune interaction may enhance immune readiness during disease-or injury-induced 'fight' responses. Research also indicate that dysregulation of the SNS can significantly affect the progression of immune-mediated diseases. However, a better understanding of neural-immune interactions is needed to develop strategies for treatment of immune-mediated diseases that are designed to return homeostasis and restore normal functioning neural-immune networks.

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Section: Functional Significance Of Sympathetic Innervation Of Secondmentioning

confidence: 99%

Sympathetic modulation of immunity: Relevance to disease

Bellinger

Millar

Perez

et al. 2008

Cellular Immunology

226

185

View full text Add to dashboard Cite

show abstract

“…17 PDE4 is also present alongside the PDE3 isoenzyme in airway smooth muscle; the PDE3 isoenzyme is considered to predominate in airway smooth muscle, and inhibition of this enzyme, rather than PDE4, inhibition of which leads to airway smooth muscle relaxation. 13 A wide range of in vitro and in vivo studies have demonstrated the ability of PDE4 inhibitors to regulate activation of relevant cells implicated in airways disease, and Table II [18][19][20][21][22][23][24][25][26][27][28][29][30][31][32][33][34][35] summarizes the various effects PDE4 inhibitors can exhibit on human inflammatory and resident cell function. PDE4 is encoded by 4 genes, each of which generates a number of isoforms that can be divided into subfamilies (PDE4A-D).…”

Section: Pde4: a Therapeutic Target In Copd And Asthmamentioning

confidence: 99%

Are phosphodiesterase 4 inhibitors just more theophylline?

Boswell-Smith

Cazzola

Page

2006

Journal of Allergy and Clinical Immunology

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“…However, there are some drawbacks in these therapies since repeated subcutaneous or intramuscular injections of these drugs are needed, there are frequent adverse reactions and quality of life is not necessarily improved by these therapies. Phosphodiesterase inhibitors suppress IFN-and TNF-, in vitro and in animal studies [190][191][192] making them candidate drugs for treating multiple sclerosis. Ibudilast has anti-inflammatory actions [193] reducing the expression of proinflammatory cytokines in patients with multiple sclerosis [189] and ameliorates neurological signs in experimental autoimmune encephalitis when administered before, but not after, the onset of disease at a serum concentration achievable with a dose close to the clinically used dose for the human diseases [194].…”

Section: Ibudilast (Av411)mentioning

confidence: 99%

Chronic Inflammatory Pain and the Neurovascular Unit: A Central Role for Glia in Maintaining BBB Integrity?

Willis

Davis²

2008

CPD

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Pain is a complex phenomenon involving both a peripheral innate immune response and a CNS response as well as activation of the hypothalamic-pituitary-adrenal axis. The peripheral innate immune response to injury involves the rapid production and local release of proinflammatory cytokines such as tumor necrosis factor-alpha (TNF-/alpha), interleukin-1 (IL-1) and IL-6. Recent studies into the CNS response to peripheral chronic inflammatory pain strongly implicates a role for glia, and local synthesis of proinflammatory cytokines and growth factors. A characteristic feature of CNS inflammation is gliosis, in which inflammatory mediators activate glial cells (e.g. astrocytes and microglia, macrophages and leukocytes) which have been shown to induce and maintain hyperalgesia. In addition, inflammatory pain induces changes in blood-brain barrier (BBB) permeability and alters transport of clinically relevant drugs used to treat pain into the brain. Despite the increasing body of evidence for the involvement of glia in chronic pain and the role of glia in maintaining the BBB, few studies have addressed glial/endothelial interactions and the mechanisms by which glia may regulate the BBB during inflammatory pain. Further studies into the cellular mechanisms of glial/endothelial interactions may identify novel therapeutic targets for reversing chronic inflammatory induced BBB dysfunction and innovate therapies for modulating the severity of chronic inflammatory pain.

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Modulation of Thl- and Th2-like cytokine production from mitogen-stimulated human peripheral blood mononuclear cells by phosphodiesterase inhibitors

Cited by 23 publications

References 22 publications

Sympathetic modulation of immunity: Relevance to disease

Sympathetic modulation of immunity: Relevance to disease

Are phosphodiesterase 4 inhibitors just more theophylline?

Chronic Inflammatory Pain and the Neurovascular Unit: A Central Role for Glia in Maintaining BBB Integrity?

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