A Review: Neutrophils, Compartmentalized Cytokine Release, and Lung Injury

Solomkin, Joseph S.; Burnett, Robert; Cave, Cynthia M.; Tindal, Carolyn J.

doi:10.1159/000424023

Cited by 3 publications

(2 citation statements)

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“…Interleukin-8 and PAF are produced by activated endothelial cells and are expressed on the cell surface where they can interact with circulating leukocytes. 20,[28][29][30][31] Human neutrophils exposed to low concentrations of IL-8 are primed, and subsequent activation of primed neutrophils results in enhanced phagocytic activity, a marked increase in oxygen radical production, and an enhanced degranulation response. 29,32 At higher concentrations, IL-8 can result in an increase in expression of adhesion molecules and can stimulate degranulation of neutrophils from several species.…”

mentioning

confidence: 99%

In vitro evaluation of the role of platelet-activating factor and interleukin-8 in Mannheimia haemolytica-induced bovine pulmonary endothelial cell injury

McClenahan¹,

Evanson²,

Weiss³

2002

ajvr

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In vitro activation of bovine macrophages by M haemolytica-derived LPS resulted in neutrophil activation and neutrophil-mediated endothelial damage. Neutrophil-mediated endothelial injury and neutrophil degranulation were, at least in part, mediated by IL8, whereas PAF promoted superoxide release by neutrophils in this in vitro system designed to mimic the in vivo events that occur during the early stages of bovine pneumonic pasteurellosis.

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confidence: 99%

In vitro evaluation of the role of platelet-activating factor and interleukin-8 in Mannheimia haemolytica-induced bovine pulmonary endothelial cell injury

McClenahan¹,

Evanson²,

Weiss³

2002

ajvr

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“…Most concepts and theories regarding the involvement of cytokines and other mediators in shock have centered upon the role of elevated plasma levels of endotoxin and secondary mediators, most notably TNF, IL-1 and IL-6 [72]. Several clinical studies have identified an association between bacteraemia, endotoxaemia, elevated cytokine plasma levels and shock.…”

Section: The Concept Of Systemic Blockadementioning

confidence: 99%

Thirty years of anti-mediator treatment in sepsis and septic shock - what have we learned?

Neugebauer

Rixen

Raum

et al. 1998

Langenbeck's Archives of Surgery

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Sepsis, the systemic response (specific and non-specific) of the body to an infection, is an increasing clinical problem. During the last 30 years, nearly 50 clinical trials involving more than 10,000 patients have failed to demonstrate improvement of patients' outcome with different "anti-mediator" strategies. The wrong conceptional approaches to interact with the complex mediator network and flaws in study design and conduct are the main reasons for this disappointing situation. We learned, however, that the systemic host response is more than persistent uncontrolled inflammation; it is also a stimulation of the counter regulatory network. Although it is important to analyse the complex picture, we have now reached a point where more sophisticated strategies for describing complexity and novel attempts for synthesis are needed. Along this line, improved study designs (decrease of "signal-to-noise ratio") are mandatory. In addition, secondary preventive strategies are emphasised.

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Retinoid-Mediated Signaling in CD38 Antigen Expression

Mehta¹

2000

Human CD38 and Related Molecules

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A Review: Neutrophils, Compartmentalized Cytokine Release, and Lung Injury

Cited by 3 publications

References 0 publications

In vitro evaluation of the role of platelet-activating factor and interleukin-8 in Mannheimia haemolytica-induced bovine pulmonary endothelial cell injury

In vitro evaluation of the role of platelet-activating factor and interleukin-8 in Mannheimia haemolytica-induced bovine pulmonary endothelial cell injury

Thirty years of anti-mediator treatment in sepsis and septic shock - what have we learned?

Retinoid-Mediated Signaling in CD38 Antigen Expression

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