Effect of β2-Adrenergic Receptor Stimulation on Interleukin-18-Induced Intercellular Adhesion Molecule-1 Expression and Cytokine Production

Takahashi, Hideo; Morichika, Toshihiko; Ishibashi, Hiromi; Yoshino, Tadashi; Tamura, Ryuji; Saito, Shinnya; Mori, Shuji; Akagi, Tadaatsu; Tanaka, Noriaki; Nishibori, Masahiro

doi:10.1124/jpet.102.042622

Cited by 31 publications

(15 citation statements)

References 41 publications

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“…*P Ͻ 0.05 vs. control mean, Dunnett's test. intercellular adhesion molecule-1 in leukocytes through a ␤ 2 -adrenergic receptor-mediated mechanism (34).…”

Section: Discussionmentioning

confidence: 99%

Adrenergic modulation ofEscherichia coliO157:H7 adherence to the colonic mucosa

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Lyte

Chen

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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Enteric neurotransmitters can modulate the biodefensive functions of the intestinal mucosa, but their role in mucosal interactions with enteropathogens is not well defined. Here we tested the hypothesis that norepinephrine (NE) modulates interactions between enterohemorrhagic Escherichia coli O157:H7 (EHEC) and the colonic epithelium. Mucosal sheets from porcine distal colon were mounted in Ussing chambers. Drugs and an inoculum of either Shiga toxin-negative or -positive EHEC were added to the contraluminal and luminal bathing medium, respectively. After 90 min, adherent bacteria were quantified by an adherence assay and by immunohistochemical methods; short-circuit current (I(sc)) was measured continuously to assess changes in active ion transport. NE-treated tissues exhibited concentration-dependent increases in I(sc) and EHEC adherence. NE did not alter adherence of a rodent-adapted, noninfectious E. coli strain or two porcine-adapted non-O157 E. coli strains. The actions of NE on EHEC adherence but not I(sc) were prevented by the alpha-adrenergic antagonist yohimbine and the PKA activator Sp-8-bromoadenosine-3',5'-cyclic monophosphorothioate. Like NE, the PKA inhibitor Rp-8-bromoadenosine-3',5'-cyclic monophosphorothioate or indirectly acting sympathomimetic agents increased EHEC adherence. Nerve fibers immunoreactive for the NE-synthesizing enzymes tyrosine hydroxylase and dopamine beta-hydroxylase appeared to innervate the colonic epithelium. EHEC-like immunoreactivity on the colonic surface had the appearance of bacterial microcolonies and increased after NE treatment by a phentolamine-sensitive mechanism. Through interactions with alpha(2)-adrenergic receptors, NE appears to increase EHEC adherence to the colonic mucosa. Changes in sympathetic neural outflow may alter intestinal susceptibility to infection.

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“…*P Ͻ 0.05 vs. control mean, Dunnett's test. intercellular adhesion molecule-1 in leukocytes through a ␤ 2 -adrenergic receptor-mediated mechanism (34).…”

Section: Discussionmentioning

confidence: 99%

Adrenergic modulation ofEscherichia coliO157:H7 adherence to the colonic mucosa

Green

Lyte

Chen

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…We found that ␤2-AR stimulation inhibited IL-18-initiated IL-12, TNF-␣ and INF-␥ production [21], and that the stimulation of ␤2-AR suppressed LPS-induced production of TNF-␣, and T cell proliferation through inhibiting the cellto-cell interaction between monocytes and T cells [22]. The purpose of the present study is to investigate the effect of ␤2-AR stimulation on IL-18 production.…”

Section: Introductionmentioning

confidence: 96%

β2-Adrenergic receptor stimulation inhibits LPS-induced IL-18 and IL-12 production in monocytes

et al. 2005

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We examined the effects of beta2-adrenergic receptor (beta2-AR) agonists on monocyte-derived cytokines, interleukin (IL)-18 and IL-12 production in lipopolysaccharide (LPS)-stimulated monocytes derived from human peripheral blood mononuclear cells (PBMCs), as in vitro model of sepsis. The study found that beta2-AR agonists inhibited IL-18 and IL-12 production in monocytes, and that AR agonist activity was antagonized by the selective beta2-AR antagonist, butoxamine. The selective beta2-AR agonists salbutamol and terbutaline induced a similar inhibitory pattern of IL-18 and IL-12 production. IL-12 production induced by LPS was inhibited by anti-IL-18 Ab, but IL-18 production by LPS was not inhibited by anti-IL-12 Ab, showing that LPS induced IL-18 production without IL-12 production. Therefore, the stimulation of beta2-AR might be beneficial in the treatment of sepsis through inhibiting LPS-elicited IL-18.

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“…It was suggested that FMF may be related to abnormal catecholamine metabolism because in these subjects a significantly higher plasma dopamine β-hydroxylase (DBH) activity was found compared with controls (Barakat et al, 1988). These irregularities in catecholamines metabolism indicate that metaraminol markedly affected immune homeostasis of the host because abnormal stimulation of adrenergic and dopaminergic receptors can lead to modulation of the cytokine network and contribute to a wide range of pathology (Agarwal & Marshall, 2000;Kohm & Sanders, 2001;Bergmann & Sautner, 2002;Takahashi et al, 2003;Johnson et al, 2005;Kaneko et al, 2005).…”

Section: Metaraminolmentioning

confidence: 94%

Mollaret Meningitis may be Caused by Reactivation of Latent Cerebral Toxoplasmosis

Prandota

2009

International Journal of Neuroscience

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Mollaret meningitis (MM) occurs mainly in females and is characterized by recurrent episodes of headache, transient neurological abnormalities, and the cerebrospinal fluid containing mononuclear cells. HSV-2 was usually identified as the causative agent. Recently, we found that recurrent headaches in non-HIV-infected subjects were due to acquired cerebral toxoplasmosis (CT). The aim of the study was therefore to focus on molecular pathomechanisms that may lead to reactivation of latent CT and manifest as MM. Literature data cited in this work were selected to illustrate that various factors may affect latent CNS Toxoplasma gondii infection/inflammation intensity and/or host defense mechanisms, i.e., the production of NO, cytokines, tryptophan degradation by indoleamine 2,3-dioxygenase, mechanisms mediated by an IFN-gamma responsive gene family, limiting the availability of intracellular iron to T. gondii, and production of reactive oxygen/nitrogen species, finally inducing choroid plexitis and/or vasculitis. Examples of triggers revealing MM and accompanying disturbances of IFN-gamma-mediated immune responses that control HSV-2 and T. gondii include: female predominance (female mice are more susceptible to T. gondii infection than males); HSV-2 infection (increased IFN-gamma, IL-12); metaraminol (increased plasma catecholamine levels, changes in cytokine expression favoring T(H)2 cells responses); probably cholesterol contained in debris from ruptured epidermoid cysts (decreased NO; increased TNF-alpha, IL-6, IL-8). These irregularities induced by the triggers may be responsible for reactivation of latent CT and development of MM. Thus, subjects with MM should have test(s) for T. gondii infection performed obligatorily.

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Effect of β2-Adrenergic Receptor Stimulation on Interleukin-18-Induced Intercellular Adhesion Molecule-1 Expression and Cytokine Production

Cited by 31 publications

References 41 publications

Adrenergic modulation ofEscherichia coliO157:H7 adherence to the colonic mucosa

Adrenergic modulation ofEscherichia coliO157:H7 adherence to the colonic mucosa

β2-Adrenergic receptor stimulation inhibits LPS-induced IL-18 and IL-12 production in monocytes

Mollaret Meningitis may be Caused by Reactivation of Latent Cerebral Toxoplasmosis

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