Dose-Response Effect of in Vivo Administration of Endotoxin on Polymorphonuclear Leukocytes Oxidative Burst

Kajdacsy-Balla, André; Doi, Elvira M.; Lerner, Megan R.; Bales, Wesley D.; Archer, L. T.; Wunder, Paulo R.; Wilson, Michael F.; Brackett, Daniel J.

doi:10.1097/00024382-199605000-00008

Cited by 10 publications

(7 citation statements)

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“…In patients with burn, trauma, or surgical procedures, neutrophils exhibited a decreased capacity to generate reactive oxygen products compared with healthy controls [17,18]. In patients with burn, trauma, or surgical procedures, neutrophils exhibited a decreased capacity to generate reactive oxygen products compared with healthy controls [17,18].…”

Section: Anaphylatoxin Impairment Of Innate Immunitymentioning

confidence: 99%

Complement-induced impairment of the innate immune system during sepsis

Albrecht

Ward

2004

Curr Allergy Asthma Rep

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The complement system is an integral part of innate immunity and is chiefly responsible for controlling bacterial infections, especially those involving gram- negative organisms. To accomplish this task, serum proteins engage in a series of enzymatic cascades. The cleaved proteins assemble pores on membranous structures, which lead to cell lysis. During this process, powerful inflammatory mediators are produced, including the anaphylatoxins, C5a, C3a, and the membrane attack complex (MAC). Under systemic inflammatory conditions, an overactive complement system may compromise the effectiveness of innate immunity. We review the detrimental effects that are caused by uncontrolled complement activation during sepsis.

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Section: Anaphylatoxin Impairment Of Innate Immunitymentioning

confidence: 99%

Complement-induced impairment of the innate immune system during sepsis

Albrecht

Ward

2004

Curr Allergy Asthma Rep

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“…In these cases, decreased oxidant generation might be due to different LPS doses or to the down-regulation that follows previous activation. Kajdacsy-Balla and co-workers [46] showed that the oxidative response of PMNs in endotoxemic rats is dependent on LPS dose and the stage of endotoxemia. For example, small doses increased superoxide release by twofold after 5 min and 10-fold by 6 h. Conversely, larger doses inhibited responses by 5 min, and oxidant releasing ability returned to normal by 3 h but never increased above control levels.…”

Section: Oxidant Productionmentioning

confidence: 99%

“…Some studies suggest that adhered or tissue-associated PMNs demonstrate even greater oxidant potential than circulating PMNs during endotoxemia [4,43,44]. However, instances of depressed or unaltered oxidant production by PMNs during endotoxemia are also reported [45][46][47]. In these cases, decreased oxidant generation might be due to different LPS doses or to the down-regulation that follows previous activation.…”

Section: Oxidant Productionmentioning

confidence: 99%

Neutrophil migration during endotoxemia

Wagner

Roth

1999

Journal of Leukocyte Biology

177

125

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Endotoxemia is marked by a global activation of inflammatory responses, which can lead to shock, multiple organ failure, and the suppression of immune and wound healing processes. Neutrophils (PMNs) play a central role in some of these responses by accumulating in tissues and releasing reactive oxygen species and proteases that injure host structures. This review focuses on altered PMN migratory responses that occur during endotoxemia and their consequences in the development of pulmonary infection. The inflammatory mediators that might be responsible for these altered responses are discussed. The oxidant potential of PMNs is increased after exposure to endotoxin both in vitro and during clinical and experimental endotoxemia. However, other functions such as chemotaxis and phagocytosis are often depressed in these same cells. Endotoxin exposure renders PMNs hyperadhesive to endothelium. The sum of these effects produces activated inflammatory cells that are incapable of leaving the vasculature. As such, the endotoxic PMN is more likely to promote tissue injury from within microvascular beds than to clear pathogens from extravascular sites. Moreover, the functional characteristics of endotoxic PMNs are similar to those observed during trauma, burn injury, sepsis, surgery, and other inflammatory conditions. Accordingly, several clinical conditions might have a common effector in the activated, yet migratorially dysfunctional, PMN. Direct effects of endotoxin on PMNs as well as effects of endogenous mediators released during endotoxemia are discussed. Understanding PMN behavior during endotoxemia may provide basic and critical insights that can be applied to a number of inflammatory scenarios. J. Leukoc. Biol. 66: 10-24; 1999.

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“…In patients with burn, trauma, or surgical procedures, neutrophils exhibited a decreased capacity to generate reactive oxygen products compared with healthy controls [17,18]. As indicated earlier, several animal studies suggest this behavior is related to C5a effects on neutrophils.…”

Section: Anaphylatoxin Impairment Of Innate Immunitymentioning

confidence: 62%