Cytokines Enhance Opsonophagocytosis of Type III Group B Streptococcus

Campbell, Judith R.; Edwards, Morven S.

doi:10.1038/sj.jp.7200360

Cited by 10 publications

(5 citation statements)

References 24 publications

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“…This marked TNF-␣ response may allow the human newborn to optimize innate immune defense against GBS in the absence of specific antibody. Consistent with this hypothesis, TNF-␣ has been shown to enhance opsonophagocytosis of GBS by human neutrophils (13), which can occur in the absence of specific antibody (10). While TNF-␣ may augment bacterial clearance by its action on neutrophils, it may also trigger the deleterious changes in host physiology associated with sepsis syndrome.…”

Section: Vol 71 2003 Role Of Complement In Gbs-induced Tnf-␣ Releasmentioning

confidence: 82%

Critical Role of the Complement System in Group BStreptococcus-Induced Tumor Necrosis Factor Alpha Release

et al. 2003

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Group B Streptococcus (GBS) is a major cause of newborn sepsis and meningitis and induces systemic release of tumor necrosis factor alpha (TNF-␣), believed to play a role in morbidity and mortality. While previous studies have shown that GBS can induce TNF-␣ release from monocytes and macrophages, little is known about the potential modulating effect of plasma or serum on GBS-induced TNF-␣ release, and there are conflicting reports as to the host receptors involved. In a human whole-blood assay system, GBS type III COH-1 potently induced substantial monocyte TNF-␣ release in adult peripheral blood and, due to a higher concentration of monocytes, 10-fold-greater TNF-␣ release in newborn cord blood. Remarkably, GBS-induced TNF-␣ release from human monocytes was enhanced ϳ1,000-fold by heat-labile serum components. Experiments employing C2-, C3-, or C7-depleted serum demonstrated that C3 activation via the alternative pathway is crucial for potent GBS-induced TNF-␣ release. Accordingly, whole blood from C3-deficient mice demonstrated significantly reduced GBS-induced TNF-␣ release. Preincubation with human serum enhanced the TNF-␣-inducing activity of GBS in a C3-and factor B-dependent manner, implying deposition of complement components via the alternative pathway. GBS-induced TNF-␣ release was inhibited by monoclonal antibodies directed against each of the components of CR3 and CR4: the common integrin ␤ subunit CD18 and the ␣ subunits CD11b (of CR3) and CD11c (of CR4). Blood derived from CR3 (CD11b/CD18)-deficient mice demonstrated a markedly diminished TNF-␣ response to GBS. We conclude that the ability of plasma and serum to greatly amplify GBS-induced TNF-␣ release reflects the activity of the alternative complement pathway that deposits fragments on GBS and thereby enhances CR3-and CR4-mediated monocyte activation.

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Section: Vol 71 2003 Role Of Complement In Gbs-induced Tnf-␣ Releasmentioning

confidence: 82%

Critical Role of the Complement System in Group BStreptococcus-Induced Tumor Necrosis Factor Alpha Release

et al. 2003

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“…GM-CSF promotes the survival, proliferation, differentiation, and activation of hematopoietic cells, predominantly in the macrophage and neutrophil lineages [54]. GM-CSF has a number of other immunomodulatory properties, including enhancement of antigen presentation, promotion of phagocytosis and antibody-dependent killing, induction of chemotaxis, and induction of the release of reactive oxygen intermediates and histamines [57][58][59][60]. It is interesting that GM-CSF is known to work synergistically with other cytokines.…”

Section: Enhancement Of Ll-37-induced Immunomodulatory Effectsmentioning

confidence: 99%

Impact of LL-37 on anti-infective immunity

Bowdish

Davidson²,

Lau

et al. 2004

Journal of Leukocyte Biology

322

295

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Host defense peptides (often called cationic antimicrobial peptides) have pleiotropic immunomodulatory functions. The human host defense peptide LL-37 is up-regulated at sites of infection and has little or no antimicrobial activity in tissue-culture media but under the same conditions, demonstrates immunomodulatory effects on epithelial cells, monocytes, and dendritic cells (DC). These effects include the induction of chemokine production in a mitogen-activated protein kinase-dependent manner in epithelial cell lines and monocytes and profound alterations of DC differentiation, resulting in the capacity to enhance a T helper cell type 1 response. Although the exact mechanisms of interaction between LL-37 and these cell types have not been elucidated, there is evidence for specific (i.e., receptor-mediated) and nonspecific interactions. The relative significance of the direct antimicrobial activities and immunomodulatory properties of LL-37 and other cationic host defense peptides in host defense remains unresolved. To demonstrate that antimicrobial activity was not necessarily required for protection in vivo, model peptides were synthesized and tested for antimicrobial and immunomodulatory activities. A peptide with no antimicrobial activity was found to be protective in animal models of Staphylococcus aureus and Salmonella infection, implying that a host defense peptide can protect by exerting immunomodulatory properties.

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“…The priming of neutrophils with growth factors or cytokines could improve the microbiocidal functions of the cells towards pathogens [ 27 , 29 , 31 ]. We thus investigated whether stimulating neutrophils with the granulocyte colony-stimulating factor (G-CSF) or the granulocyte-macrophage colony-stimulating factor (GM-CSF)–two growth factors essential for neutrophil control—could improve cell efficacy to kill S .…”

Section: Resultsmentioning

confidence: 99%

“…Among the priming agents, granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) regulate neutrophils at several levels and functions [18,19]. Most studies used "chemical" agonists as a second step of activation (or activation agent) [18][19][20][21][22][23][24][25][26], while only few studies evaluated the effect of priming on the response to pathogens [27][28][29][30][31][32].…”

Section: Introductionmentioning

confidence: 99%

Encapsulated Streptococcus suis impairs optimal neutrophil functions which are not rescued by priming with colony-stimulating factors

Bleuzé,

Lavoie,

Bédard

et al. 2024

PLoS ONE

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The porcine pathogen and zoonotic agent Streptococcus suis induces an exacerbated inflammation in the infected hosts that leads to sepsis, meningitis, and sudden death. Several virulence factors were described for S. suis of which the capsular polysaccharide (CPS) conceals it from the immune system, and the suilysin exhibits cytotoxic activity. Although neutrophils are recruited rapidly upon S. suis infection, their microbicidal functions appear to be poorly activated against the bacteria. However, during disease, the inflammatory environment could promote neutrophil activation as mediators such as the granulocyte colony-stimulating factor granulocyte (G-CSF) and the granulocyte-macrophages colony-stimulating factor (GM-CSF) prime neutrophils and enhance their responsiveness to bacterial detection. Thus, we hypothesized that CPS and suilysin prevent an efficient activation of neutrophils by S. suis, but that G-CSF and GM-CSF rescue neutrophil activation, leading to S. suis elimination. We evaluated the functions of porcine neutrophils in vitro in response to S. suis and investigated the role of the CPS and suilysin on cell activation using isogenic mutants of the bacteria. We also studied the influence of G-CSF and GM-CSF on neutrophil response to S. suis by priming the cells with recombinant proteins. Our study confirmed that CPS prevents S. suis-induced activation of most neutrophil functions but participates in the release of neutrophil-extracellular traps (NETs). Priming with G-CSF did not influence cell activation, but GM-CSF strongly promote IL-8 release, indicating its involvement in immunomodulation. However, priming did not enhance microbicidal functions. Studying the interaction between S. suis and neutrophils–first responders in host defense–remains fundamental to understand the immunopathogenesis of the infection and to develop therapeutical strategies related to neutrophils’ defense against this bacterium.

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Cytokines Enhance Opsonophagocytosis of Type III Group B Streptococcus

Cited by 10 publications

References 24 publications

Critical Role of the Complement System in Group BStreptococcus-Induced Tumor Necrosis Factor Alpha Release

Critical Role of the Complement System in Group BStreptococcus-Induced Tumor Necrosis Factor Alpha Release

Impact of LL-37 on anti-infective immunity

Encapsulated Streptococcus suis impairs optimal neutrophil functions which are not rescued by priming with colony-stimulating factors

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