Blood inflammatory response to inhaled endotoxin in normal subjects

Blood inflammatory response to inhaled endotoxin in normal subjects Summary Previously we have reported that in asthmatics an inhalation of 20 μg lipopolysaccharide (LPS) produces a bronchial obstruction associated with an inflammatory blood response. The aim of the present study was to evaluate this response in normal subjects. Eight normal non‐atopic subjects were challenged by inhalation of a solution containing 20 μg LPS (from Escherichia coli 026:B6) a week after bronchial challenge with control solution. The lung function response was evaluated by the changes in forced expiratory volume in one second (FEV1), in specific conductance and in airway resistance while the blood inflammatory response was evaluated by serial measures of total white blood cells (WBC) and polymorphonuclear neutrophils (PMN) count, luminol enhanced‐chemiluminescence (luminol‐CL, as a marker of the PMN degree of activation), C‐reactive protein (CRP), haptoglobin, complement fraction C3, tumour necrosis factor‐α (TNF‐α) and adrenocorticotropic hormone (ACTH). No response in lung function was observed for 6 h after the LPS inhalation. The count in WBC and PMN increased 300 (P < 0.01) and 360 (P < 0.01) min after the LPS challenge associated with an increase in the level of luminol‐CL (P < 0.001). This rise in luminol‐CL level was significant at 120 min (P < 0.05) before any change in the PMN count. After 24 and 48 h the acute‐phase protein CRP raised significantly (P < 0.01), the other proteins C3 and haptoglobin being unchanged. A slight increase in ACTH was observed 240 and 360 min (P < 0.05) after the LPS challenge while the TNFα detectable level was not modified. In conclusion, in normal subjects, inhalation of a pro‐inflammatory agent is able to induce a systemic inflammatory response in the absence of any effect on lung mechanics, while in asthmatics the same bronchial challenge has been reported to induce a similar blood inflammation associated with a significant response in lung function. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Clinical & Experimental Allergy Wiley

Blood inflammatory response to inhaled endotoxin in normal subjects

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Publisher
Wiley
Copyright
Copyright © 1995 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0954-7894
eISSN
1365-2222
DOI
10.1111/j.1365-2222.1995.tb01005.x
Publisher site
See Article on Publisher Site

Abstract

Summary Previously we have reported that in asthmatics an inhalation of 20 μg lipopolysaccharide (LPS) produces a bronchial obstruction associated with an inflammatory blood response. The aim of the present study was to evaluate this response in normal subjects. Eight normal non‐atopic subjects were challenged by inhalation of a solution containing 20 μg LPS (from Escherichia coli 026:B6) a week after bronchial challenge with control solution. The lung function response was evaluated by the changes in forced expiratory volume in one second (FEV1), in specific conductance and in airway resistance while the blood inflammatory response was evaluated by serial measures of total white blood cells (WBC) and polymorphonuclear neutrophils (PMN) count, luminol enhanced‐chemiluminescence (luminol‐CL, as a marker of the PMN degree of activation), C‐reactive protein (CRP), haptoglobin, complement fraction C3, tumour necrosis factor‐α (TNF‐α) and adrenocorticotropic hormone (ACTH). No response in lung function was observed for 6 h after the LPS inhalation. The count in WBC and PMN increased 300 (P < 0.01) and 360 (P < 0.01) min after the LPS challenge associated with an increase in the level of luminol‐CL (P < 0.001). This rise in luminol‐CL level was significant at 120 min (P < 0.05) before any change in the PMN count. After 24 and 48 h the acute‐phase protein CRP raised significantly (P < 0.01), the other proteins C3 and haptoglobin being unchanged. A slight increase in ACTH was observed 240 and 360 min (P < 0.05) after the LPS challenge while the TNFα detectable level was not modified. In conclusion, in normal subjects, inhalation of a pro‐inflammatory agent is able to induce a systemic inflammatory response in the absence of any effect on lung mechanics, while in asthmatics the same bronchial challenge has been reported to induce a similar blood inflammation associated with a significant response in lung function.

Journal

Clinical & Experimental AllergyWiley

Published: Jan 1, 1995

References

  • Effect of corticosteroid treatment on interleukin‐1 and tumour necrosis factor secretion by monocytes from subjects with asthma
    Vecchariarelli, Vecchariarelli; Siracusa, Siracusa; Cenci, Cenci; Puliti, Puliti; Abbritti, Abbritti
  • Domestic endotoxin exposure and clinical severity of asthma
    Michel, Michel; Ginanni, Ginanni; Duchateau, Duchateau
  • Effects of inhaled endotoxin on bronchial reactivity in asthmatic and normal subjects
    Michel, Michel; Duchateau, Duchateau; Sergysels, Sergysels
  • Dissociation between plasma and monocyte‐association cytokines during sepsis
    Munoz, Munoz; Misset, Misset; Fitting, Fitting; Bleriot, Bleriot; Carlet, Carlet; Cavaillon, Cavaillon

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