Differential inflammatory response to inhaled lipopolysaccharide targeted either to the airways or the alveoli in man.

Endotoxin (Lipopolysaccharide, LPS) is a potent inducer of inflammation and there is various LPS contamination in the environment, being a trigger of lung diseases and exacerbation. The objective of this study was to assess the time course of inflammation and the sensitivities of the airways and alv...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Winfried Möller, Irene Heimbeck, Thomas P J Hofer, Gülnaz Khadem Saba, Margot Neiswirth, Marion Frankenberger, Löms Ziegler-Heitbrock
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2012
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/2bab047863f246ca8d4745b397aae0a0
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:2bab047863f246ca8d4745b397aae0a0
record_format	dspace
spelling	oai:doaj.org-article:2bab047863f246ca8d4745b397aae0a02021-11-18T07:23:18ZDifferential inflammatory response to inhaled lipopolysaccharide targeted either to the airways or the alveoli in man.1932-620310.1371/journal.pone.0033505https://doaj.org/article/2bab047863f246ca8d4745b397aae0a02012-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/22496751/?tool=EBIhttps://doaj.org/toc/1932-6203Endotoxin (Lipopolysaccharide, LPS) is a potent inducer of inflammation and there is various LPS contamination in the environment, being a trigger of lung diseases and exacerbation. The objective of this study was to assess the time course of inflammation and the sensitivities of the airways and alveoli to targeted LPS inhalation in order to understand the role of LPS challenge in airway disease.In healthy volunteers without any bronchial hyperresponsiveness we targeted sequentially 1, 5 and 20 µg LPS to the airways and 5 µg LPS to the alveoli using controlled aerosol bolus inhalation. Inflammatory parameters were assessed during a 72 h time period. LPS deposited in the airways induced dose dependent systemic responses with increases of blood neutrophils (peaking at 6 h), Interleukin-6 (peaking at 6 h), body temperature (peaking at 12 h), and CRP (peaking at 24 h). 5 µg LPS targeted to the alveoli caused significantly stronger effects compared to 5 µg airway LPS deposition. Local responses were studied by measuring lung function (FEV(1)) and reactive oxygen production, assessed by hydrogen peroxide (H(2)O(2)) in fractionated exhaled breath condensate (EBC). FEV(1) showed a dose dependent decline, with lowest values at 12 h post LPS challenge. There was a significant 2-fold H(2)O(2) induction in airway-EBC at 2 h post LPS inhalation. Alveolar LPS targeting resulted in the induction of very low levels of EBC-H(2)O(2).Targeting LPS to the alveoli leads to stronger systemic responses compared to airway LPS targeting. Targeted LPS inhalation may provide a novel model of airway inflammation for studying the role of LPS contamination of air pollution in lung diseases, exacerbation and anti-inflammatory drugs.Winfried MöllerIrene HeimbeckThomas P J HoferGülnaz Khadem SabaMargot NeiswirthMarion FrankenbergerLöms Ziegler-HeitbrockPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 7, Iss 4, p e33505 (2012)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Winfried Möller Irene Heimbeck Thomas P J Hofer Gülnaz Khadem Saba Margot Neiswirth Marion Frankenberger Löms Ziegler-Heitbrock Differential inflammatory response to inhaled lipopolysaccharide targeted either to the airways or the alveoli in man.
description	Endotoxin (Lipopolysaccharide, LPS) is a potent inducer of inflammation and there is various LPS contamination in the environment, being a trigger of lung diseases and exacerbation. The objective of this study was to assess the time course of inflammation and the sensitivities of the airways and alveoli to targeted LPS inhalation in order to understand the role of LPS challenge in airway disease.In healthy volunteers without any bronchial hyperresponsiveness we targeted sequentially 1, 5 and 20 µg LPS to the airways and 5 µg LPS to the alveoli using controlled aerosol bolus inhalation. Inflammatory parameters were assessed during a 72 h time period. LPS deposited in the airways induced dose dependent systemic responses with increases of blood neutrophils (peaking at 6 h), Interleukin-6 (peaking at 6 h), body temperature (peaking at 12 h), and CRP (peaking at 24 h). 5 µg LPS targeted to the alveoli caused significantly stronger effects compared to 5 µg airway LPS deposition. Local responses were studied by measuring lung function (FEV(1)) and reactive oxygen production, assessed by hydrogen peroxide (H(2)O(2)) in fractionated exhaled breath condensate (EBC). FEV(1) showed a dose dependent decline, with lowest values at 12 h post LPS challenge. There was a significant 2-fold H(2)O(2) induction in airway-EBC at 2 h post LPS inhalation. Alveolar LPS targeting resulted in the induction of very low levels of EBC-H(2)O(2).Targeting LPS to the alveoli leads to stronger systemic responses compared to airway LPS targeting. Targeted LPS inhalation may provide a novel model of airway inflammation for studying the role of LPS contamination of air pollution in lung diseases, exacerbation and anti-inflammatory drugs.
format	article
author	Winfried Möller Irene Heimbeck Thomas P J Hofer Gülnaz Khadem Saba Margot Neiswirth Marion Frankenberger Löms Ziegler-Heitbrock
author_facet	Winfried Möller Irene Heimbeck Thomas P J Hofer Gülnaz Khadem Saba Margot Neiswirth Marion Frankenberger Löms Ziegler-Heitbrock
author_sort	Winfried Möller
title	Differential inflammatory response to inhaled lipopolysaccharide targeted either to the airways or the alveoli in man.
title_short	Differential inflammatory response to inhaled lipopolysaccharide targeted either to the airways or the alveoli in man.
title_full	Differential inflammatory response to inhaled lipopolysaccharide targeted either to the airways or the alveoli in man.
title_fullStr	Differential inflammatory response to inhaled lipopolysaccharide targeted either to the airways or the alveoli in man.
title_full_unstemmed	Differential inflammatory response to inhaled lipopolysaccharide targeted either to the airways or the alveoli in man.
title_sort	differential inflammatory response to inhaled lipopolysaccharide targeted either to the airways or the alveoli in man.
publisher	Public Library of Science (PLoS)
publishDate	2012
url	https://doaj.org/article/2bab047863f246ca8d4745b397aae0a0
work_keys_str_mv	AT winfriedmoller differentialinflammatoryresponsetoinhaledlipopolysaccharidetargetedeithertotheairwaysorthealveoliinman AT ireneheimbeck differentialinflammatoryresponsetoinhaledlipopolysaccharidetargetedeithertotheairwaysorthealveoliinman AT thomaspjhofer differentialinflammatoryresponsetoinhaledlipopolysaccharidetargetedeithertotheairwaysorthealveoliinman AT gulnazkhademsaba differentialinflammatoryresponsetoinhaledlipopolysaccharidetargetedeithertotheairwaysorthealveoliinman AT margotneiswirth differentialinflammatoryresponsetoinhaledlipopolysaccharidetargetedeithertotheairwaysorthealveoliinman AT marionfrankenberger differentialinflammatoryresponsetoinhaledlipopolysaccharidetargetedeithertotheairwaysorthealveoliinman AT lomszieglerheitbrock differentialinflammatoryresponsetoinhaledlipopolysaccharidetargetedeithertotheairwaysorthealveoliinman
_version_	1718423524363730944

Differential inflammatory response to inhaled lipopolysaccharide targeted either to the airways or the alveoli in man.

Ejemplares similares