Phagocytic function of polymorphonuclear leukocytes and the RES in endotoxemia

Regel, G.; Nerlich, Michael; Dwenger, A.; Seidel, J.; Schmidt, Cornelia; Sturm, J. A.

doi:10.1016/0022-4804(87)90068-0

Cited by 30 publications

(22 citation statements)

References 33 publications

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“…The present study confirms previous reports of decreased levels of chemotaxis (2), phagocytosis (20), ROI production (19,22,24,25), and killing (16,17) in neutrophils from septicemic subjects. For patients with septicemia, methods using whole blood and assays with isolated cells yielded similar results for neutrophil phagocytosis and ROI production.…”

supporting

confidence: 93%

“…Various neutrophil functions have been described as being reduced in sepsis, including adherence (21), chemotaxis (2), degranulation (20), phagocytosis (17), and production of reactive oxygen intermediates (ROI) (19,24,25). However, other studies have reported enhanced neutrophil chemotaxis and respiratory burst activities, particularly in patients without underlying conditions (8,10,12).…”

mentioning

confidence: 99%

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Assessment of Neutrophil Function in Patients with Septic Shock: Comparison of Methods

Wenisch

Fladerer

Patruta

et al. 2001

Clin Diagn Lab Immunol

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Patients with septic shock are shown to have decreased neutrophil phagocytic function by multiple assays, and their assessment by whole-blood assays (fluorescence-activated cell sorter analysis) correlates with assays requiring isolated neutrophils (microscopic and spectrophotometric assays). For patients with similar underlying conditions but without septic shock, this correlation does not occur.

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supporting

confidence: 93%

mentioning

confidence: 99%

Assessment of Neutrophil Function in Patients with Septic Shock: Comparison of Methods

Wenisch

Fladerer

Patruta

et al. 2001

Clin Diagn Lab Immunol

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“…In addition, phagocytic killing of yeast is increased in PMNs from endotoxemic rats [49]. This is in contrast to results in an ovine model in which phagocytosis-associated bactericidal and candidicidal activities are depressed by 15 min after endotoxin administration [50]. Furthermore, studies in endotoxemic rats and humans show no changes in phagocytic function of circulating PMNs [22,51].…”

Section: Phagocytosismentioning

confidence: 86%

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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“…Impairment of granulocyte function results in an impaired host defense against invading microorganisms (8,29). During infection, a reduction of various granulocyte functions has been demonstrated (12,33,43,44,46), whereas an increased ROI production was observed in patients with acute pancreatitis (39). Alteration of the nonspecific host defense by antibiotics has received increasing interest in the past few years (8).…”

Section: Discussionmentioning

confidence: 99%

“…Neutrophil adherence (44), chemotaxis (12), phagocytosis (33), and the production of reactive oxygen intermediates (ROI) (43) were diminished during the acute inflammatory response. In addition, plasma isolated from patients with septic shock and incubated with normal neutrophils significantly inhibited superoxide anion production (46).…”

mentioning

confidence: 99%

Effect of cefodizime and ceftriaxone on phagocytic function in patients with severe infections

Wenisch

Parschalk

Hasenhündl

et al. 1995

Antimicrob Agents Chemother

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Thirty patients with severe bacterial infections were treated with 50 mg of cefodizime per kg of body weight once daily or 50 mg of ceftriaxone per kg once daily for 10 ؎ 3 days. The effect of cefodizime and ceftriaxone on the phagocytic capacity and generation of reactive oxygen intermediates after phagocytosis by granulocytes was assessed prior to, during, and after therapy. Flow cytometry was used to study phagocytic capacity by measuring the uptake of fluorescein-labeled bacteria. The generation of reactive oxygen intermediates after phagocytosis was estimated by the quantification of the intracellular conversion of dihydrorhodamine 123 to rhodamine 123. Prior to therapy, patients in both groups exhibited a decreased capacity to phagocytize Escherichia coli and subsequently to generate reactive oxygen intermediates. Granulocyte function increased after the initiation of therapy and normalized within 7 days for the ceftriaxone-treated patients and within 3 days for the cefodizime group (P < 0.05). In the cefodizime group, an enhancement of phagocytic capacity was observed 14 days after the initiation of therapy (P < 0.05). Prior to therapy, phagocytic capacity was significantly correlated with the generation of reactive oxygen products (r ‫؍‬ 0.674 and P < 0.005).

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Phagocytic function of polymorphonuclear leukocytes and the RES in endotoxemia

Cited by 30 publications

References 33 publications

Assessment of Neutrophil Function in Patients with Septic Shock: Comparison of Methods

Assessment of Neutrophil Function in Patients with Septic Shock: Comparison of Methods

Neutrophil migration during endotoxemia

Effect of cefodizime and ceftriaxone on phagocytic function in patients with severe infections

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