Differential effect of prostaglandins E1 and E2 on lipopolysaccharide-induced adhesion molecule expression on human monocytes

Takahashi, Hideo; Ishibashi, Hiromi; Tamura, Ryuji; Katsuno, Goutaro; Dong, Xue; Sugita, Sachi; Mori, Shuji; Yoshino, Tadashi; Tanaka, Noriaki; Nishibori, Masahiro

doi:10.1016/j.ejphar.2005.01.046

Cited by 14 publications

(11 citation statements)

References 32 publications

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“…production in peripheral blood mononuclear cells (PBMC), but it had no effect on the production of interleukin (IL)-18, IL-12, and interferon (IFN)-+ (10). Moreover, LPS at 1 ng/mL upregulated the expression of intercellular adhesion molecule (ICAM)-1, B7.1, B7.2, and CD40 on monocytes (10,11). Antibodies (Abs) against ICAM-1, B7.1, and CD40 abolished the LPS-initiated TNF-!…”

Section: Introductionmentioning

confidence: 98%

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Stimulation of Α7 Nicotinic Acetylcholine Receptor Inhibits Cd14 and the Toll-Like Receptor 4 Expression in Human Monocytes

Hamano

Takahashi

Ishibashi

et al. 2006

Shock

Self Cite

105

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The lipopolysaccharide (LPS)-receptor complex, CD14/toll-like receptor 4, is known to play a role in the immune responses during sepsis. Excessive inflammation and tumor necrosis factor (TNF)-alpha synthesis have been reported to cause morbidity and mortality in endotoxemia and sepsis. Cell-to-cell interaction through the engagement between intercellular adhesion molecule 1, B7.1, and CD40 on monocytes and their ligands on T cells has been suggested to play a role in the inflammatory response such as TNF-alpha and interleukin 10 production. Nicotine, with the stimulation of the nicotinic acetylcholine receptor alpha7 subunit (alpha7-nAChR), has now become the focus of attention because of its anti-inflammatory effects. However, little is known about the mechanism of the inhibitory effects induced by nicotine on the LPS-induced immune responses. In the present study, we found that nicotine suppressed the expression of CD14, toll-like receptor 4, intercellular adhesion molecule 1, B7.1, and CD40 on monocytes and the production of TNF-alpha, but not interleukin 10, in human peripheral blood mononuclear cells in the presence of LPS. The actions of nicotine were reversed by a nonselective and a selective alpha7-nAChR antagonist, mecamylamine and alpha-bungarotoxin, respectively. Therefore, nicotine might inhibit the LPS receptor complex expression via alpha7-nAChR, thus leading to a decrease in the adhesion molecule expression and TNF-alpha production. Moreover, we demonstrated that a nuclear factor-kappaB and a p38 mitogen-activated protein kinase inhibitor mimicked the actions of nicotine in the presence of LPS. These results suggested that the nuclear factor-kappaB and p38 mitogen-activated protein kinase might be involved in the actions of nicotine.

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Section: Introductionmentioning

confidence: 98%

“…production in PBMC, thus suggesting that the engagement of adhesion molecules is involved in LPS-induced TNF-! production (10,11). Recombinant IL-10 potently suppresses LPS-induced production of TNF-!, and pretreatment with IL-10 inhibits TNF-!…”

Section: Introductionmentioning

confidence: 99%

Stimulation of Α7 Nicotinic Acetylcholine Receptor Inhibits Cd14 and the Toll-Like Receptor 4 Expression in Human Monocytes

Hamano

Takahashi

Ishibashi

et al. 2006

Shock

Self Cite

105

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“…26,27 In primary cells, agonist doses between 0.1 and 10 M are reportedly sufficient to elicit maximal functional and signaling responses. 28,29 Each selective reagent was dissolved in dimethyl sulfoxide (DMSO; Sigma, St Louis, MO). Pertussis toxin (PTX) was purchased from Sigma.…”

Section: Methodsmentioning

confidence: 99%

Human mast cells express multiple EP receptors for prostaglandin E2 that differentially modulate activation responses

Cheng

Beller

Bagga

et al. 2006

Blood

124

135

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“…PGE 2 is often regarded as a proinflammatory mediator (27). However, it may also possess potent antiinflammatory properties (28)(29)(30)(31). To establish whether the NSAID-mediated reduction in PGE 2 was responsible for the NSAID-mediated rise in spontaneous TNF production, exogenous PGE 2 (5 mM) was added to NSAID-treated rheumatoid synovial membrane cell cultures.…”

Section: Nsaid Induced Changes In Tnf Are Seen In Response To a Variementioning

confidence: 99%

Nonsteroidal Anti-Inflammatory Drugs Increase TNF Production in Rheumatoid Synovial Membrane Cultures and Whole Blood

Page

Turner

Brown

et al. 2010

The Journal of Immunology

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Differential effect of prostaglandins E1 and E2 on lipopolysaccharide-induced adhesion molecule expression on human monocytes

Cited by 14 publications

References 32 publications

Stimulation of Α7 Nicotinic Acetylcholine Receptor Inhibits Cd14 and the Toll-Like Receptor 4 Expression in Human Monocytes

Stimulation of Α7 Nicotinic Acetylcholine Receptor Inhibits Cd14 and the Toll-Like Receptor 4 Expression in Human Monocytes

Human mast cells express multiple EP receptors for prostaglandin E2 that differentially modulate activation responses

Nonsteroidal Anti-Inflammatory Drugs Increase TNF Production in Rheumatoid Synovial Membrane Cultures and Whole Blood

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