Induction of cyclooxygenase-2 by human monocytes exposed to group B streptococci

Maloney, Christopher G.; Thompson, Samuel D.; Hill, Harry R.; Bohnsack, John F.; McIntyre, Thomas M.; Zimmerman, Guy A.

doi:10.1002/jlb.67.5.615

Cited by 22 publications

(17 citation statements)

References 41 publications

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“…Consequently, it is time-consuming, laborious and hardly feasible in routine clinical practice, as treatment is usually started without prior platelet function testing. In our study, the vast majority of patients received endothelium, may contribute to the observed association [34][35][36] . The weaker impact of inflammation on serum TXB2 also supports the assumption that extraplatelet sources play a role in the strong correlation between inflammation and urinary D-TXB2.…”

Section: Supplementary Tablementioning

confidence: 61%

Differential Impact of Inflammation on Six Laboratory Assays Measuring Residual Arachidonic Acid-Inducible Platelet Reactivity During Dual Antiplatelet Therapy

Gremmel

Perkmann

Seidinger

et al. 2013

JAT

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Aims: Inflammation has been postulated to modify the platelet response to aspirin treatment, thereby causing high on-treatment residual platelet reactivity (HRPR). Both high levels of inflammatory markers and HRPR have been linked to adverse cardiovascular events. We aimed to study the impact of inflammation on residual arachidonic acid (AA)-inducible platelet reactivity. Methods: In 288 patients receiving dual antiplatelet therapy, residual AA-inducible platelet reactivity was assessed using light transmission aggregometry (LTA), the VerifyNow assay, multiple electrode aggregometry (MEA) and the Impact-R. The levels of urinary 11-dehydro-thromboxane B2 (D-TXB2), serum thromboxane B2 (TXB2), interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hsCRP) were determined using immunoassays. Results: The IL-6 level was found to be an independent predictor of platelet reactivity as determined according to LTA and D-TXB2 using a multiple linear regression analysis. Accordingly, patients with supramedian IL-6 levels exhibited significantly higher platelet reactivity than patients with inframedian IL-6 levels when determined according to LTA and D-TXB2 (both p ≤ 0.02). High IL-6 levels were associated with a 3.6-fold (95%CI 2.1-6.4) increased risk of HRPR, as defined according to D-TXB2, and a 3.4-fold (95%CI 1.4-8.3) increased risk of HRPR, as defined according to MEA. The HsCRP level was found to be an independent predictor of platelet reactivity when determined according to LTA, D-TXB2, the Impact-R and TXB2 using a multiple linear regression analysis. High hsCRP levels were associated with a 3.6-fold (95%CI 1.3-10) increased risk of HRPR, as defined according to LTA, and a 2.5-fold (95%CI 1.3-4.6) increased risk of HRPR, as defined according to TXB2. Conclusions: Increased levels of inflammatory markers are independently associated with residual AA-inducible platelet reactivity in patients receiving dual antiplatelet treatment.

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Section: Supplementary Tablementioning

confidence: 61%

Differential Impact of Inflammation on Six Laboratory Assays Measuring Residual Arachidonic Acid-Inducible Platelet Reactivity During Dual Antiplatelet Therapy

Gremmel

Perkmann

Seidinger

et al. 2013

JAT

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“…Early-onset GBS pneumonia is characterized by presence of numerous bacteria, an inflammatory exudate, and marked pulmonary epithelial and endothelial cell injury (1,10). Innate proinflammatory responses to GBS infection which may contribute to the respiratory pathology include the synthesis and release of cytokines (12,22), prostaglandins (16), and nitric oxide (NO) (6,15).…”

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confidence: 99%

Cytokine Responses to Group B Streptococci Induce Nitric Oxide Production in Respiratory Epithelial Cells

Goodrum

Poulson-Dunlap

2002

Infect Immun

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Streptococcus agalactiae (group B streptococcus [GBS]) is a leading cause of neonatal pneumonia, sepsis, and meningitis. Early-onset GBS pneumonia is characterized by marked pulmonary epithelial and endothelial cell injury. Innate proinflammatory responses to GBS infection that may contribute to the respiratory pathology include the synthesis and release of cytokines, prostaglandins, and nitric oxide (NO). The hypothesis that NO is directly induced in lung epithelial cells by invading GBS or indirectly induced by cytokines released by GBS-infected mononuclear cells was tested. A549 transformed human respiratory epithelial cells were directly cultured with GBS, cocultured with GBS-infected human mononuclear cells or purified macrophages, or exposed to conditioned culture medium from human mononuclear cells infected by GBS. The culture medium of A549 cultures was assayed for NO secretion, and the cell lysates were tested for presence of inducible nitric oxide synthase (iNOS) mRNA by reverse transcriptase PCR (RT-PCR). GBS-treated A549 cells neither secreted detectable NO nor expressed iNOS mRNA. GBS interaction with human mononuclear cells, however, stimulated release of soluble factors that readily induced iNOS mRNA expression and NO secretion by A549 cells. Inflammatory mediator-induced nitric oxide (NO) production by alveolar epithelium may exceed that of other lung cell types such as macrophages, and induction during GBS infection may play a significant role in pulmonary defense or free-radical-mediated lung injury. Streptococcus agalactiae (group B streptococcus [GBS]) is a leading cause of neonatal pneumonia, sepsis, and meningitis (26). GBS is also an important pathogen in maternal infections and in infections of nonpregnant adults with risk factors such as older age and underlying disorders (25). Early-onset GBS pneumonia is characterized by presence of numerous bacteria, an inflammatory exudate, and marked pulmonary epithelial and endothelial cell injury (1, 10). Innate proinflammatory responses to GBS infection which may contribute to the respiratory pathology include the synthesis and release of cytokines (12,22), prostaglandins (16), and nitric oxide (NO) (6, 15).In the lung, alveolar macrophages, airway epithelial cells, endothelial cells, and inflammatory cells may be sources for NO (24). Though GBS, with or without cytokines, has been shown to induce NO production in cultured murine macrophages (3,6,20), human macrophages produce far less NO (5-to 100-fold less) in response to cytokine or microbial stimuli than do murine macrophages (31). An alternate source of alveolar NO are human lung epithelial cells, which possess a nitric oxide synthase (iNOS, NOS2) that is inducible by a mixture of cytokines (21) that should, based on in vitro data, be released locally by GBS-infected alveolar macrophages and mononuclear cells (12). Alternatively, direct GBS invasion of respiratory epithelial cells (23) might also induce NO production.In this report, human respiratory epithelial cells were directly cultured w...

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“…Effective first-line defense must be established in the earliest stages of microbial invasion, before the microbial sensing system is overwhelmed by large numbers of invading bacteria (Medzhitov and Janeway, 2000). At the same time, innate proinflammatory response to GBS infection may contribute to bacterial pathology through the synthesis and release of cytokines, prostaglandins and nitric oxide (Kwak et al, 2000;Leib et al, 1998;Maloney et al, 2000). It appears therefore that the virulence of different strains may be due not only to different genotypes but also to the induction of different amounts of proinflammatory cytokines.…”

Section: Introductionmentioning

confidence: 99%

Different Sequence Strains ofStreptococcus agalactiaeElicit Various Levels of Cytokine Production

Francesco

Gargiulo

Negrini

et al. 2008

Immunological Investigations

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Group B streptococcus (GBS) is the most common cause of neonatal and obstetric sepsis and an increasingly important cause of septicemia in elderly subjects and immunocompromised patients. Our aim was to evaluate whether different genotypes of GBS may induce a different production of pro-inflammatory and anti-inflammatory cytokines. We used multilocus sequence typing to identify 71 clones isolated from asymptomatic healthy carriers and symptomatic individuals. All these clinical isolates were used to infect purified human monocytes. TNF-alpha, IL-6, IL-8 and IL-10 secretion was measured. Fifteen allelic sequence types (STs) were identified. The MLST (multilocus sequence typing) analysis grouped the bacteria into four different lineages (clonal cluster) and two of these were closely involved in the infection of symptomatic subjects: CC17 and CC19. Furthermore, CC17 and CC19 stimulated TNF-alpha, IL-6 and IL-8 production significantly more than the other lineages, while CC17 induced a decreased IL-10 production. These results suggest the existence of differences in immune response to infection with particular genotypes of GBS.

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Induction of cyclooxygenase-2 by human monocytes exposed to group B streptococci

Cited by 22 publications

References 41 publications

Differential Impact of Inflammation on Six Laboratory Assays Measuring Residual Arachidonic Acid-Inducible Platelet Reactivity During Dual Antiplatelet Therapy

Differential Impact of Inflammation on Six Laboratory Assays Measuring Residual Arachidonic Acid-Inducible Platelet Reactivity During Dual Antiplatelet Therapy

Cytokine Responses to Group B Streptococci Induce Nitric Oxide Production in Respiratory Epithelial Cells

Different Sequence Strains ofStreptococcus agalactiaeElicit Various Levels of Cytokine Production

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