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Transcompartmental Inflammatory Responses in Humans: IV Versus Endobronchial Administration of Endotoxin

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Standard

Transcompartmental Inflammatory Responses in Humans : IV Versus Endobronchial Administration of Endotoxin. / Plovsing, Ronni R; Berg, Ronan M G; Evans, Kevin A; Konge, Lars; Iversen, Martin; Garred, Peter; Møller, Kirsten.

I: Critical Care Medicine, Bind 42, Nr. 7, 07.2014, s. 1658–1665.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Plovsing, RR, Berg, RMG, Evans, KA, Konge, L, Iversen, M, Garred, P & Møller, K 2014, 'Transcompartmental Inflammatory Responses in Humans: IV Versus Endobronchial Administration of Endotoxin', Critical Care Medicine, bind 42, nr. 7, s. 1658–1665. https://doi.org/10.1097/CCM.0000000000000320

APA

Plovsing, R. R., Berg, R. M. G., Evans, K. A., Konge, L., Iversen, M., Garred, P., & Møller, K. (2014). Transcompartmental Inflammatory Responses in Humans: IV Versus Endobronchial Administration of Endotoxin. Critical Care Medicine, 42(7), 1658–1665. https://doi.org/10.1097/CCM.0000000000000320

Vancouver

Plovsing RR, Berg RMG, Evans KA, Konge L, Iversen M, Garred P o.a. Transcompartmental Inflammatory Responses in Humans: IV Versus Endobronchial Administration of Endotoxin. Critical Care Medicine. 2014 jul;42(7):1658–1665. https://doi.org/10.1097/CCM.0000000000000320

Author

Plovsing, Ronni R ; Berg, Ronan M G ; Evans, Kevin A ; Konge, Lars ; Iversen, Martin ; Garred, Peter ; Møller, Kirsten. / Transcompartmental Inflammatory Responses in Humans : IV Versus Endobronchial Administration of Endotoxin. I: Critical Care Medicine. 2014 ; Bind 42, Nr. 7. s. 1658–1665.

Bibtex

@article{0652a61803524f2aae61ed8b99ad71bb,
title = "Transcompartmental Inflammatory Responses in Humans: IV Versus Endobronchial Administration of Endotoxin",
abstract = "OBJECTIVES: Transcompartmental signaling during early inflammation may lead to propagation of disease to other organs. The time course and the mechanisms involved are still poorly understood. We aimed at comparing acute transcompartmental inflammatory responses in humans following lipopolysaccharide-induced pulmonary and systemic inflammation.DESIGN: Randomized, double-blind, placebo-controlled, crossover study.SETTING ICU SUBJECTS: Healthy male volunteers.INTERVENTIONS: Fifteen volunteers (mean age, 23; SD, 2 yr) received Escherichia coli endotoxin (lipopolysaccharide, 4 ng/kg) IV or endobronchially on two different study days. Groups were evaluated by bronchoalveolar lavage at baseline (0 hr) and 2, 4, 6, 8, or 24 hours postchallenge. Cardiorespiratory variables were continuously recorded throughout the study day, and plasma and bronchoalveolar lavage fluid markers of inflammation were measured.MEASUREMENTS AND MAIN RESULTS: IV endotoxin elicited a systemic inflammatory response with a time-dependent increase and peak in tumor necrosis factor-α, interleukin-6, and leukocyte counts (all p < 0.001). Furthermore, a delayed (6-8 hr) increase in bronchoalveolar lavage fluid interleukin-6 concentration (p < 0.001) and alveolar leukocyte count (p = 0.03) and a minor increase in bronchoalveolar lavage fluid tumor necrosis factor-α were observed (p = 0.06). Endobronchial endotoxin was followed by progressive alveolar neutrocytosis and increased bronchoalveolar lavage fluid tumor necrosis factor-α, interleukin-6, and albumin (all p < 0.001); a systemic inflammatory response was observed after 2-4 hours, with no change in plasma tumor necrosis factor-α.CONCLUSIONS: Acute lung or systemic inflammation in humans is followed by a transcompartmental proinflammatory response, the degree and differential kinetics of which suggests that the propagation of inflammation may depend on the primary site of injury.",
keywords = "Acute Lung Injury, Administration, Intravenous, Adult, Biological Markers, Bronchoalveolar Lavage, Double-Blind Method, Drug Administration Routes, Endotoxins, Hemodynamics, Humans, Inflammation, Inflammation Mediators, Lipopolysaccharides, Lung Diseases, Male, Pneumonia, Systemic Inflammatory Response Syndrome, Time Factors",
author = "Plovsing, {Ronni R} and Berg, {Ronan M G} and Evans, {Kevin A} and Lars Konge and Martin Iversen and Peter Garred and Kirsten M{\o}ller",
year = "2014",
month = jul,
doi = "10.1097/CCM.0000000000000320",
language = "English",
volume = "42",
pages = "1658–1665",
journal = "Critical Care Medicine",
issn = "0090-3493",
publisher = "Lippincott Williams & Wilkins",
number = "7",

}

RIS

TY - JOUR

T1 - Transcompartmental Inflammatory Responses in Humans

T2 - IV Versus Endobronchial Administration of Endotoxin

AU - Plovsing, Ronni R

AU - Berg, Ronan M G

AU - Evans, Kevin A

AU - Konge, Lars

AU - Iversen, Martin

AU - Garred, Peter

AU - Møller, Kirsten

PY - 2014/7

Y1 - 2014/7

N2 - OBJECTIVES: Transcompartmental signaling during early inflammation may lead to propagation of disease to other organs. The time course and the mechanisms involved are still poorly understood. We aimed at comparing acute transcompartmental inflammatory responses in humans following lipopolysaccharide-induced pulmonary and systemic inflammation.DESIGN: Randomized, double-blind, placebo-controlled, crossover study.SETTING ICU SUBJECTS: Healthy male volunteers.INTERVENTIONS: Fifteen volunteers (mean age, 23; SD, 2 yr) received Escherichia coli endotoxin (lipopolysaccharide, 4 ng/kg) IV or endobronchially on two different study days. Groups were evaluated by bronchoalveolar lavage at baseline (0 hr) and 2, 4, 6, 8, or 24 hours postchallenge. Cardiorespiratory variables were continuously recorded throughout the study day, and plasma and bronchoalveolar lavage fluid markers of inflammation were measured.MEASUREMENTS AND MAIN RESULTS: IV endotoxin elicited a systemic inflammatory response with a time-dependent increase and peak in tumor necrosis factor-α, interleukin-6, and leukocyte counts (all p < 0.001). Furthermore, a delayed (6-8 hr) increase in bronchoalveolar lavage fluid interleukin-6 concentration (p < 0.001) and alveolar leukocyte count (p = 0.03) and a minor increase in bronchoalveolar lavage fluid tumor necrosis factor-α were observed (p = 0.06). Endobronchial endotoxin was followed by progressive alveolar neutrocytosis and increased bronchoalveolar lavage fluid tumor necrosis factor-α, interleukin-6, and albumin (all p < 0.001); a systemic inflammatory response was observed after 2-4 hours, with no change in plasma tumor necrosis factor-α.CONCLUSIONS: Acute lung or systemic inflammation in humans is followed by a transcompartmental proinflammatory response, the degree and differential kinetics of which suggests that the propagation of inflammation may depend on the primary site of injury.

AB - OBJECTIVES: Transcompartmental signaling during early inflammation may lead to propagation of disease to other organs. The time course and the mechanisms involved are still poorly understood. We aimed at comparing acute transcompartmental inflammatory responses in humans following lipopolysaccharide-induced pulmonary and systemic inflammation.DESIGN: Randomized, double-blind, placebo-controlled, crossover study.SETTING ICU SUBJECTS: Healthy male volunteers.INTERVENTIONS: Fifteen volunteers (mean age, 23; SD, 2 yr) received Escherichia coli endotoxin (lipopolysaccharide, 4 ng/kg) IV or endobronchially on two different study days. Groups were evaluated by bronchoalveolar lavage at baseline (0 hr) and 2, 4, 6, 8, or 24 hours postchallenge. Cardiorespiratory variables were continuously recorded throughout the study day, and plasma and bronchoalveolar lavage fluid markers of inflammation were measured.MEASUREMENTS AND MAIN RESULTS: IV endotoxin elicited a systemic inflammatory response with a time-dependent increase and peak in tumor necrosis factor-α, interleukin-6, and leukocyte counts (all p < 0.001). Furthermore, a delayed (6-8 hr) increase in bronchoalveolar lavage fluid interleukin-6 concentration (p < 0.001) and alveolar leukocyte count (p = 0.03) and a minor increase in bronchoalveolar lavage fluid tumor necrosis factor-α were observed (p = 0.06). Endobronchial endotoxin was followed by progressive alveolar neutrocytosis and increased bronchoalveolar lavage fluid tumor necrosis factor-α, interleukin-6, and albumin (all p < 0.001); a systemic inflammatory response was observed after 2-4 hours, with no change in plasma tumor necrosis factor-α.CONCLUSIONS: Acute lung or systemic inflammation in humans is followed by a transcompartmental proinflammatory response, the degree and differential kinetics of which suggests that the propagation of inflammation may depend on the primary site of injury.

KW - Acute Lung Injury

KW - Administration, Intravenous

KW - Adult

KW - Biological Markers

KW - Bronchoalveolar Lavage

KW - Double-Blind Method

KW - Drug Administration Routes

KW - Endotoxins

KW - Hemodynamics

KW - Humans

KW - Inflammation

KW - Inflammation Mediators

KW - Lipopolysaccharides

KW - Lung Diseases

KW - Male

KW - Pneumonia

KW - Systemic Inflammatory Response Syndrome

KW - Time Factors

U2 - 10.1097/CCM.0000000000000320

DO - 10.1097/CCM.0000000000000320

M3 - Journal article

C2 - 24732241

VL - 42

SP - 1658

EP - 1665

JO - Critical Care Medicine

JF - Critical Care Medicine

SN - 0090-3493

IS - 7

ER -

ID: 138503268