Group B streptococci and inducible nitric oxide synthase: Modulation by nuclear factor kappa B and ibuprofen

Glibetić, Maria; Samlalsingh-Parker, Jacqueline; Raykova, Vania; Ofenstein, John P.; Aranda, Jacob V.

doi:10.1053/sper.2001.23181

Cited by 20 publications

(11 citation statements)

References 25 publications

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“…It is known that b-h/c contributes significantly to mortality in adult mice in association with the production of proinflammatory cytokines such as IL-1a and IL-6 [11]. Expression of these 2 cytokines typically reflects activation of NF-kB pathways, and NF-kB activation has recently been shown to be an early step in the induction of iNOS gene expression by GBS [12].…”

Section: Discussionmentioning

confidence: 98%

Synergistic Action of Nitric Oxide Release from Murine Macrophages Caused by Group B Streptococcal Cell Wall and β‐Hemolysin/Cytolysin

et al. 2002

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Group B streptococcus (GBS) is the leading cause of sepsis in neonates. Nitric oxide (NO) release plays a role in the hypotension that characterizes septic shock. It has been shown that GBS beta-hemolysin/cytolysin (beta-h/c) stimulates the transcription of inducible NO synthase (iNOS) in murine macrophages via intracellular pathways similar to those that mediate lipopolysaccharide-induced iNOS activation. Here, it is demonstrated that the GBS cell wall and beta-h/c act synergistically to induce iNOS in interferon (IFN)-gamma-primed [corrected] RAW 264.7 murine macrophages. In nonprimed macrophages, combined activation by the GBS cell wall plus beta-h/c is necessary to induce an NO response, which indicates that both virulence factors cooperate to substitute for the priming signal typically provided by IFN-gamma [corrected].

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Section: Discussionmentioning

confidence: 98%

Synergistic Action of Nitric Oxide Release from Murine Macrophages Caused by Group B Streptococcal Cell Wall and β‐Hemolysin/Cytolysin

et al. 2002

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“…Many signaling cascades may be involved in the promotion of inflammatory conditions and the induction of adhesion molecules in the endothelium, among which the activation of the transcription factor NF-kB and the subsequent induction of iNOS and NO, play a major role [24][25][26]. In addition, signaling mechanisms via cell surface receptors coupled to intracellular calcium transients (Ca ++ ), stimulating cNOS-derived NO release, are major players in limiting endothelium activation since the NO so produced stabilizes NF-kB, prevents its further activation and expression of adhesion molecules [27].…”

Section: Discussionmentioning

confidence: 99%

Selective serotonin re-uptake inhibitors decrease the cytokine-induced endothelial adhesion molecule expression, the endothelial adhesiveness to monocytes and the circulating levels of vascular adhesion molecules

Lekakis

Ikonomidis

Papoutsi

et al. 2010

International Journal of Cardiology

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“…For example, Kopp & Ghosh (1994) found that sodium salicylate is capable of inhibiting NF‐ κ B activation. Glibetic et al . (2001) showed that NF‐ κ B activation is an early step in the induction of iNOS gene expression by Group B streptococci, and that ibuprofen suppressed GBS‐induced iNOS mRNA expression blocking NF‐ κ B activation.…”

Section: Discussionmentioning

confidence: 99%

Effects of cyclooxygenase inhibitor pretreatment on nitric oxide production, nNOS and iNOS expression in rat cerebellum

Girolamo

Farina

Riberio

et al. 2003

British J Pharmacology

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1 The therapeutic effect of nonsteroidal anti-inflammatory drugs (NSAIDs) is thought to be due mainly to its inhibition of cyclooxygenase (COX) enzymes, but there is a growing body of research that now demonstrates a variety of NSAIDs effects on cellular signal transduction pathways other than those involving prostaglandins. 2 Nitric oxide (NO) as a free radical and an agent that gives rise to highly toxic oxidants (peroxynitrile, nitric dioxide, nitron ion), becomes a cause of neuronal damage and death in some brain lesions such as Parkinson and Alzheimer disease, and Huntington's chorea. 3 In the present study, the in vivo effect of three NSAIDs (lysine clonixinate (LC), indomethacine (INDO) and meloxicam (MELO)) on NO production and nitric oxide synthase expression in rat cerebellar slices was analysed. Rats were treated with (a) saline, (b) lipopolysaccharide (LPS) (5 mg kg À1 , i.p.), (c) saline in combination with different doses of NSAIDs and (d) LPS in combination with different doses of NSAIDs and then killed 6 h after treatment. 4 NO synthesis, evaluated by Bred and Snyder technique, was increased by LPS. This augmentation was inhibited by coadministration of the three NSAIDs assayed. None of the NSAIDs tested was able to modify control NO synthesis. 5 Expression of iNOS and neural NOS (nNOS) was detected by Western blotting in control and LPS-treated rats. LC and INDO, but not MELO, were able to inhibit the expression of these enzymes. 6 Therefore, reduction of iNOS and nNOS levels in cerebellum may explain, in part, the antiinflammatory effect of these NSAIDs and may also have importance in the prevention of NOmediated neuronal injury.

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Group B streptococci and inducible nitric oxide synthase: Modulation by nuclear factor kappa B and ibuprofen

Cited by 20 publications

References 25 publications

Synergistic Action of Nitric Oxide Release from Murine Macrophages Caused by Group B Streptococcal Cell Wall and β‐Hemolysin/Cytolysin

Synergistic Action of Nitric Oxide Release from Murine Macrophages Caused by Group B Streptococcal Cell Wall and β‐Hemolysin/Cytolysin

Selective serotonin re-uptake inhibitors decrease the cytokine-induced endothelial adhesion molecule expression, the endothelial adhesiveness to monocytes and the circulating levels of vascular adhesion molecules

Effects of cyclooxygenase inhibitor pretreatment on nitric oxide production, nNOS and iNOS expression in rat cerebellum

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