Platelets augment respiratory burst in neutrophils activated by selected species of gram-positive or gram-negative bacteria.

Międzobrodzki, Jacek; Panz, Tomasz; Płonka, Przemysław M.; Zając, Katarzyna; Dracz, Joanna; Pytel, Kamila M; Mateuszuk, Łukasz; Chłopicki, Stefan

doi:10.2478/v10042-008-0052-1

Cited by 21 publications

(14 citation statements)

References 22 publications

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“…In line with our findings, it has also been reported that S. aureus triggers CD11b upregulation and oxidative burst (40). Furthermore, phagocytosis was recently implicated as a crucial event of the innate immune response to S. aureus (22,41).…”

Section: Discussionsupporting

confidence: 92%

Combined Inhibition of Complement and CD14 Efficiently Attenuated the Inflammatory Response Induced byStaphylococcus aureusin a Human Whole Blood Model

Skjeflo

Christiansen

Espevik

et al. 2014

The Journal of Immunology

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The complement and TLR systems are activated in sepsis, contributing to an unfavorable inflammatory “storm.” Combined inhibition of these systems has been documented to efficiently attenuate the inflammatory responses induced by Gram-negative bacteria. In this study, we hypothesized that the combined inhibition would attenuate the inflammatory responses induced by Gram-positive bacteria. Staphylococcus aureus bacteria (strains Cowan and Wood), as well as S. aureus cell wall lipoteichoic acid (LTA), were incubated in thrombin-inhibited human whole blood. Complement was inhibited at the level of C3 and C5, and the TLRs by inhibiting CD14 and TLR2. Thirty-four inflammatory markers were measured by multiplex technology and flow cytometry. Thirteen markers increased significantly in response to Cowan and Wood, and 12 in response to LTA. Combined inhibition with the C3 inhibitor compstatin and the anti-CD14 Ab 18D11 significantly reduced 92 (Cowan, LTA) and 85% (Wood) of these markers. Compstatin alone significantly reduced 54 (Cowan), 38 (Wood), and 83% (LTA), whereas anti-CD14 alone significantly reduced 23, 15, and 67%, respectively. Further experiments showed that the effects of complement inhibition were mainly due to inhibition of C5a interaction with the C5a receptor. The effects on inhibiting CD14 and TLR2 were similar. The combined regimen was more efficient toward the bacterial effects than either complement or anti-CD14 inhibition alone. Complement was responsible for activation of and phagocytosis by both granulocytes and monocytes. Disrupting upstream recognition by inhibiting complement and CD14 efficiently attenuated S. aureus–induced inflammation and might be a promising treatment in both Gram-negative and Gram-positive sepsis.

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Section: Discussionsupporting

confidence: 92%

Combined Inhibition of Complement and CD14 Efficiently Attenuated the Inflammatory Response Induced byStaphylococcus aureusin a Human Whole Blood Model

Skjeflo

Christiansen

Espevik

et al. 2014

The Journal of Immunology

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“…These findings suggest that MAP kinase pathways are in play in COX-2 and PGE 2 production, but not IL-6 expression in these cells. In related studies, platelets have been shown to enhance neutrophil oxidative burst in response to Gram-positive as well as Gram-negative bacteria [42]. Moreover, Bennett et al demonstrated that platelets participate in the regulation of B- and T-lymphocyte- and immunoglobulin-mediated immune responses via CD40/ligand–CD40 interactions [9].…”

Section: Platelets: the Other White Cellsmentioning

confidence: 99%

Platelets in defense against bacterial pathogens

Yeaman

2009

Cell. Mol. Life Sci.

255

234

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Platelets interact with bacterial pathogens through a wide array of cellular and molecular mechanisms. The consequences of this interaction may significantly influence the balance between infection and immunity. On the one hand, recent data indicate that certain bacteria may be capable of exploiting these interactions to gain a virulence advantage. Indeed, certain bacterial pathogens appear to have evolved specific ways in which to subvert activated platelets. Hence, it is conceivable that some bacterial pathogens exploit platelet responses. On the other hand, platelets are now known to possess unambiguous structures and functions of host defense effector cells. Recent discoveries emphasize critical features enabling such functions, including expression of toll-like receptors that detect hallmark signals of bacterial infection, an array of microbicidal peptides, as well as other host defense molecules and functions. These concepts are consistent with increased risk and severity of bacterial infection as correlates of clinical abnormalities in platelet quantity and quality. In these respects, the molecular and cellular roles of platelets in host defense against bacterial pathogens are explored with attention on advances in platelet immunobiology.

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“…Platelets, which bind more avidly to the endothelium after TLR4 stimulation, can snare neutrophils via P-selectin-PSGL-1 interactions, allowing for secondary interactions between neutrophils and the endothelium via lymphocyte function-associated antigen 1. In addition to enhancing neutrophil recruitment into infected tissues, platelets also enhance the bactericidal activity of neutrophils by increasing levels of TNF (7,28,77) and by secreting IL-1␤ (46) and thromboxane A 2 (TXA 2 ), which enhances the respiratory burst activity of neutrophils (56). Antibody blockade of P-selectin decreases neutrophil infiltration and bacterial clearance in a rat model of cecal ligation and puncture (CLP) (64), supporting an in vivo role for platelet P-selectin in host defense.…”

Section: Plateletsmentioning

confidence: 99%

Inflection points in sepsis biology: from local defense to systemic organ injury

Seeley

Matthay

Wolters

2012

American Journal of Physiology-Lung Cellular and Molecular Phys

108

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Sepsis and septic shock lead to considerable morbidity and mortality in developed and developing countries. Despite advances in understanding the innate immune events that lead to septic shock, molecular therapies based on these advances have failed to improve sepsis mortality. The clinical failure of laboratory-derived therapies may be, in part, due to the pleiotropic consequences of the acute inflammatory response, which is the focus of this review. A brisk response to infecting organism is essential for pathogen containment and eradication. However, systemic spread of inflammation beyond a single focus leads to organ injury and higher mortality. The primary goal of this article is to discuss recent animal- and human-based scientific advances in understanding the host response to infection and to highlight how these defense mechanisms can be locally beneficial but systemically detrimental. There are other factors that determine the severity of sepsis that are beyond the scope of this review, including the virulence of the pathogen and regulation by Toll-like receptors. Specifically, this review focuses on how the effector mechanisms of platelets, mast cells, neutrophil extracellular traps (NETs), and the endothelium participate in combating local infections yet can induce organ injury during systemic infection.

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Platelets augment respiratory burst in neutrophils activated by selected species of gram-positive or gram-negative bacteria.

Cited by 21 publications

References 22 publications

Combined Inhibition of Complement and CD14 Efficiently Attenuated the Inflammatory Response Induced byStaphylococcus aureusin a Human Whole Blood Model

Combined Inhibition of Complement and CD14 Efficiently Attenuated the Inflammatory Response Induced byStaphylococcus aureusin a Human Whole Blood Model

Platelets in defense against bacterial pathogens

Inflection points in sepsis biology: from local defense to systemic organ injury

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