Production of nitrite by primary rat astrocytes in response to pneumococci

Bernatowicz, Andrea; Ködel, Uwe; Frei, Karl; Fontana, Adriano; Pfister, Hans‐Walter

doi:10.1016/0165-5728(95)00053-5

Cited by 30 publications

(18 citation statements)

References 33 publications

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“…These findings differ from studies of the response of glial cells and astrocytes to pneumococci. For example, Bernatowicz et al [19] stimulated astrocyte cultures with 10 6 -10 8 cfu/mL heat-killed unencapsulated pneumococci alone and found significantly increased NO accumulation after 24-72 h of incubation. Likewise, Kim et al [20] found that purified pneumococcal cell walls (without rIFN-g) stimulated astrocytes and microglia to produce NO.…”

Section: Discussionmentioning

confidence: 97%

“…The few recent studies that have evaluated NO or iNOS production in response to pneumococci have used rat central nervous system cells (astrocytes and microglia) [19][20][21]. No information is available regarding the ability of pneumococci or its components to at Northern Arizona University on May 30, 2015 http://jid.oxfordjournals.org/ Downloaded from trigger NO or iNOS production by macrophages, the cells that play a critical role in the host response to sepsis.…”

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confidence: 99%

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Pneumococci Stimulate the Production of the Inducible Nitric Oxide Synthase and Nitric Oxide by Murine Macrophages

1998

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The role of nitric oxide (NO) in the pathophysiology of gram-positive sepsis is uncertain. In inflammatory conditions, high-output NO production is catalyzed by the enzyme inducible nitric oxide synthase (iNOS). The ability of 2 strains of pneumococci, pneumococcal cell wall preparations, and purified pneumococcal capsule (Pnu-Imune 23) to trigger the production of iNOS protein and NO in RAW 264.7 murine macrophages was tested. Live pneumococci, oxacillin-killed pneumococci, and pneumococcal cell wall preparations stimulated the production of iNOS and NO by RAW 264.7 cells in the presence, but not the absence, of low concentrations of recombinant murine interferon-gamma. In contrast, purified pneumococcal capsule induced little or no iNOS or NO production by these cells. Thus, pneumococci stimulate high-output NO production by murine macrophages. The potential role of NO in the pathogenesis of pneumococcal sepsis deserves further study.

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Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 99%

Pneumococci Stimulate the Production of the Inducible Nitric Oxide Synthase and Nitric Oxide by Murine Macrophages

1998

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“…The presence of GABA, an inhibitory neurotransmitter, may contribute to control of childhood convulsions and epilepsy [9]. L-canavanine also is of interest, since earlier studies showed that this compound could suppress NO accumulation in astrocytes [35]. Furthermore, the presence of triterpenes could account for its effects upon adrenocorticosteroid metabolism, and reduction of corticosterone levels and treatment of anxiety and stress [2].…”

Section: Discussionmentioning

confidence: 99%

Sutherlandia frutescens Ethanol Extracts Inhibit Oxidative Stress and Inflammatory Responses in Neurons and Microglial Cells

et al. 2014

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Sutherlandia frutescens (L.) R.Br. (SF) is a medicinal plant indigenous to southern Africa and used in folk and contemporary remedies for stress, chronic diseases, cancer, and HIV/AIDS. While previous studies have focused on physiological effects of SF on cellular and systemic abnormalities associated with these diseases, little is known about its effects in the brain and immune cells in the central nervous system. Results of this study indicate that ethanol extracts of SF (SF-E) suppress NMDA-induced reactive oxygen species (ROS) production in neurons, and LPS- and IFNγ-induced ROS and nitric oxide (NO) production in microglial cells. SF-E’s action on microglial cells appears to be mediated through inhibition of the IFNγ-induced p-ERK1/2 signaling pathway which is central to regulating a number of intracellular metabolic processes including enhancing STAT1α phosphorylation and filopodia formation. The involvement of SF in these pathways suggests the potential for novel therapeutics for stress and prevention, and/or treatment of HIV/AIDS as well as other inflammatory diseases in the brain.

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“…Dexamethasone acts on multiple molecules of the TLR downstream signaling cascade, including TAK-1, ERK1/2, MAPK, NF-B, and STAT3 (41,542). Astroglial cells stimulated with PCW components produced decreased amounts of NO and TNF-␣ when they were treated with dexamethasone (38,154,444). Brain microvascular endothelial cells also showed reduced levels of TNF-␣ and IL-1 and decreased expression of ICAM-1 (153).…”

Section: Adjunctive Dexamethasone Therapymentioning

confidence: 99%

Pathogenesis and Pathophysiology of Pneumococcal Meningitis

et al. 2011

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SUMMARY Pneumococcal meningitis continues to be associated with high rates of mortality and long-term neurological sequelae. The most common route of infection starts by nasopharyngeal colonization by Streptococcus pneumoniae , which must avoid mucosal entrapment and evade the host immune system after local activation. During invasive disease, pneumococcal epithelial adhesion is followed by bloodstream invasion and activation of the complement and coagulation systems. The release of inflammatory mediators facilitates pneumococcal crossing of the blood-brain barrier into the brain, where the bacteria multiply freely and trigger activation of circulating antigen-presenting cells and resident microglial cells. The resulting massive inflammation leads to further neutrophil recruitment and inflammation, resulting in the well-known features of bacterial meningitis, including cerebrospinal fluid pleocytosis, cochlear damage, cerebral edema, hydrocephalus, and cerebrovascular complications. Experimental animal models continue to further our understanding of the pathophysiology of pneumococcal meningitis and provide the platform for the development of new adjuvant treatments and antimicrobial therapy. This review discusses the most recent views on the pathophysiology of pneumococcal meningitis, as well as potential targets for (adjunctive) therapy.

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Production of nitrite by primary rat astrocytes in response to pneumococci

Cited by 30 publications

References 33 publications

Pneumococci Stimulate the Production of the Inducible Nitric Oxide Synthase and Nitric Oxide by Murine Macrophages

Pneumococci Stimulate the Production of the Inducible Nitric Oxide Synthase and Nitric Oxide by Murine Macrophages

Sutherlandia frutescens Ethanol Extracts Inhibit Oxidative Stress and Inflammatory Responses in Neurons and Microglial Cells

Pathogenesis and Pathophysiology of Pneumococcal Meningitis

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