Comparison of agents producing a neutrophilic leukocytosis in man. Hydrocortisone, prednisone, endotoxin, and etiocholanolone.

Dale, DC; Fauci, Anthony S.; Wolff, SheldonM.

doi:10.1172/jci108159

Cited by 297 publications

(101 citation statements)

References 24 publications

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“…The observed rapid increase in bone marrow neutrophil production can only be explained by an increased rate of release of these preformed neutrophils, given an anticipated delay of 3-4 days before increased proliferation within the mitotic pool would be expected to contribute (43). The overall 2.46 Ϯ 0.42-fold increment in circulating neutrophil numbers observed was consistent with other studies investigating acute mobilization of neutrophils from the bone marrow reserve (12,23,33), suggesting that the response to such leukocytosis-inducing stimuli is of a relatively uniform magnitude. The progressive increase in relative size of the younger CD10 Ϫ /CD16 low subpopulation during net circulating neutrophil pool growth was consistent with age-dependent first in-first out kinetics for neutrophil release from the bone marrow.…”

Section: Discussionsupporting

confidence: 88%

A kinetic model of bone marrow neutrophil production that characterizes late phenotypic maturation

Orr¹,

Wilson²,

Taylor³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Acute inflammatory stimuli rapidly mobilize neutrophils from the bone marrow by shortening postmitotic maturation time and releasing younger neutrophils; however, the kinetics of this change in maturation time remains unknown. We propose a kinetic model that examines the rate of change in neutrophil average age at exit from the bone marrow during active mobilization to quantify this response and use this model to examine the temporal profile of late neutrophil phenotypic maturation. Total and CD10−/CD16lowcirculating neutrophils were quantified in cardiac surgery patients during extracorporeal circulation (ECC). Net growth in the circulating neutrophil pool occurred during the procedural (0.04 ± 0.02 × 109·l−1·min−1), warming (0.14 ± 0.02 × 109·l−1·min−1), and weaning (0.12 ± 0.06 × 109·l−1·min−1) phases of ECC. When applied to our differential equation mathematical model, these results predict that neutrophil average age at exit from the bone marrow decreased continually during ECC, resulting in average neutrophil release 8.44 ± 2.20 h earlier during the weaning phase than at the beginning of ECC sampling. Modeling of concurrent changes in CD10−/CD16lowneutrophil numbers indicates that CD10 expression is directly related to neutrophil mean age and predicts that the proportion of mobilizable postmitotic neutrophils that are CD10+increases from 64 to 81% during these sampled 8.4 h of maturation.

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Section: Discussionsupporting

confidence: 88%

A kinetic model of bone marrow neutrophil production that characterizes late phenotypic maturation

Orr¹,

Wilson²,

Taylor³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…We also evaluated for any active medications with leukocytosis as a known side effect, including glucocorticoids [19], lithium [20], and recombinant colony-stimulating factors rG-CSF and rGM-CSF. Patients with any of the above conditions or medications were excluded.…”

Section: Population and Data Collectionmentioning

confidence: 99%

Clinical outcomes of ED patients with bandemia

Shi¹,

Vilke²,

Coyne³

et al. 2015

The American Journal of Emergency Medicine

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Background: Although an elevated white blood cell count is a widely utilized measure for evidence of infection and an important criterion for evaluation of systemic inflammatory response syndrome, its component band count occupies a more contested position within clinical emergency medicine. Recent studies indicate that bandemia is highly predictive of a serious infection, suggesting that clinicians who do not appreciate the value of band counts may delay diagnosis or overlook severe infections. Objectives: Whereas previous studies focused on determining the quantitative value of the band count (ie, determining sensitivity, threshold for bandemia, etc.), this study directs attention to patient-centered outcomes, hypothesizing that the degree of bandemia predisposes patients to subsequent negative clinical outcomes associated with underappreciated severe infections. Methods: This retrospective study of electronic medical records includes patients who initially presented to the emergency department (ED) with bandemia and were subsequently discharged from the ED. These patients were screened for repeat ED visits within 7 days and death within 30 days. Results: In patients with severe bandemia who were discharged from the ED, there was a 20.9% revisit rate at 7 days and a 4.9% mortality rate at 30 days, placing severely bandemic patients at 5 times significantly greater mortality compared to nonbandemic patients (P = .032). Conclusion: Our review of patient outcomes suggests that the degree of bandemia, especially in the setting of concurrent tachycardia or fever, is associated with greater likelihood of negative clinical outcomes.

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“…However, despite the strong capacity of GCS to inhibit inflammation, inhibition of neutrophil-driven inflammation seems to be less effective [19]. Other studies have shown that GCSs elicit proinflammatory effects on granulocytes, such as increased interleukin (IL)-1 receptor (IL-1R) type I expression on human neutrophils [20], prolonged neutrophil survival in vitro [21,22], leukocytosis in vivo [23], p38 activation in neutrophils and eosinophils [24,25], increased immunoglobulin A binding by eosinophils [25], and increased secretion of lysosomal enzymes by neutrophils [26]. Because not only proinflammatory, but also anti-inflammatory, mediators are controlled by the transcription factor NF-kB, GCSs would be expected to affect the expression of anti-inflammatory response as well, which is not often assessed.…”

mentioning

confidence: 99%

Steroids induce a disequilibrium of secreted interleukin-1 receptor antagonist and interleukin-1 synthesis by human neutrophils

Langereis

Oudijk²,

Schweizer³

et al. 2010

European Respiratory Journal

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Chronic obstructive pulmonary disease (COPD) is characterised by neutrophilic inflammation in the airways and these neutrophils contribute to the production of inflammatory mediators. Dampening the production of proinflammatory mediators might be an important strategy to treat COPD and glucocorticosteroids are known to do so via inhibition of nuclear factor-kB. However, this pathway is important for the control of pro-and anti-inflammatory genes.We studied the effects of dexamethasone on production and secretion of pro-inflammatory interleukin (IL)-1b and anti-inflammatory secreted IL-1 receptor antagonist (sIL-1Ra) by human neutrophils activated with tumor necrosis factor (TNF)-a.In vitro, TNF-a-stimulated neutrophils produced significant amounts of IL-1b and sIL-1Ra; this production was inhibited by dexamethasone. However, synthesis and secretion of sIL-1Ra was inhibited at lower concentrations dexamethasone compared to IL-1b, which changed the IL-1b:sIL1Ra ratio significantly. This altered ratio resulted in a more pro-inflammatory condition, as visualised by increased intercellular adhesion molecule-1 expression on human endothelial cells. In vivo, moderate-to-severe COPD patients using inhaled glucocorticosteroids have decreased plasma sILRa levels compared with mild-to-moderate patients not on glucocorticosteroid treatment.In conclusion, dexamethasone induces a pro-inflammatory shift in the IL-1b:sIL-1Ra cytokine balance in neutrophils in vitro, which might contribute to a lack of endogenous anti-inflammatory signals to dampen inflammation in vivo.

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Comparison of agents producing a neutrophilic leukocytosis in man. Hydrocortisone, prednisone, endotoxin, and etiocholanolone.

Cited by 297 publications

References 24 publications

A kinetic model of bone marrow neutrophil production that characterizes late phenotypic maturation

A kinetic model of bone marrow neutrophil production that characterizes late phenotypic maturation

Clinical outcomes of ED patients with bandemia

Steroids induce a disequilibrium of secreted interleukin-1 receptor antagonist and interleukin-1 synthesis by human neutrophils

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