Endotoxin is thought to contribute to pulmonary hyperresponsiveness in byssinosis, asthma, and the acute respiratory distress syndrome (ARDS). The aim of this study was to elucidate the mechanism of this phenomenon in the isolated, blood-free perfused mouse lung. Perfusion with lipopolysaccharide (LPS) had no effect on pulmonary resistance or pulmonary artery pressure, but induced airway hyperreactivity (AHR) to methacholine (MCh) and pulmonary vascular hyperreactivity (VHR) to platelet-activating factor (PAF). Blockade of the thromboxane/endoperoxide (TP) receptor with SQ29.548 completely protected against LPS-induced AHR and VHR. Blockade of cyclooxygenase-2 (COX-2) abolished LPS-induced VHR but suppressed LPS-induced AHR only marginally. COX-2 messenger RNA was upregulated in LPS-treated lungs, and inhibition of transcription with actinomycin D or of protein biosynthesis with cycloheximide protected against LPS-induced VHR but not AHR. Pretreatment with the radical scavenger N-acetylcysteine partly pro...

https://www.atsjournals.org/doi/pdf/10.1164/ajrccm.162.4.9912079

Mechanisms of endotoxin-induced airway and pulmonary vascular hyperreactivity in mice

Expression of peripheral blood lymphocyte muscarinic cholinergic receptor subtypes in airway hyperresponsiveness

Immunopharmacological Approach to Elucidating the Mechanism of Allergic Inflammation

Background: The role of 5-lipoxygenase (5-LO) products in the asthmatic bronchoconstriction is evident. However, the role of 5-LO products in airway hyperresponsiveness (AHR) and ai

The effect of leukotriene D (4) inhalation on the antigen-induced airway hyperresponsiveness and inflammation in 5-lipoxygenase gene-deficient mice

Endotoxin (ET) contaminated dusts frequently can be found in the environment. Especially in agriculture, ETs represent one of the main factors in the development of respiratory diseases. In order to investigate the pathomechanisms of ET induced lung injury, the contribution of the NANC-system of vagal C-fibres to increased airway responsiveness (AR) to cholinergic agents was investigated in anesthetized rabbits. In two control groups of 6 anesthetized Wight New Zealand rabbits each, E. coli ET was infused i.v. (0.4microg/kg) (Group 1) or the aerosolized ET was inhaled for 10 min (Group 2). Before and 1 and 3 hours after ET exposure, AR to 0.2 und 2.0% acetylcholine aerosol was measured. The increased AR after ET application was compared with the ET responses in rabbits with neuropeptides depleted by subchronic capsaicin treatment on four consecutive days (Groups 3 and 4). ET-inhalation and ET-infusion both resulted in a significant increase in AR to ACH (P<0.005). The increase in dynamic elastance (E(dyn)), as a measure of airway resistance to 0.2% ACH after ET in both groups was comparable with the response to 2.0% ACH before exposure. In rabbits with capsaicin treatment, basal ACH-responsiveness was similar to the control group. After ET-Exposure, increase in AR to ACH was significantly (P<0.05) smaller compared with untreated rabbits. In conclusion, depletion of neuropeptides by capsaicin resulted in a significantly decreased ET-induced airway hyperresponsiveness (AHR) in rabbits, indicating the contribution of the NANC-system and their neuromodulators to ET-induced AHR. The results confirm the important role of the NANC-system environmental and occupational agents induced-AHR in rabbits.

/pdf/endotoxin-induced-airway-hyperresponsiveness-in-rabbits-11d3topce1.pdf

Endotoxin-induced airway hyperresponsiveness in rabbits: contribution of neuropeptides.

In guinea pigs, a marked increase in airway responsiveness to acetylcholine (Ach) was observed at 2 h after lipopolysaccharide (LPS) inhalation. To examine the mediators responsible for the airway hyperresponsiveness, the changes of peptide-leukotrienes (LTs), tumor necrosis factor (TNF), interleukin-1 (IL-1), histamine and 5-hydroxytryptamine (5-HT) levels in bronchoalveolar lavage fluid (BALF) were measured. Airway responsiveness to Ach reached a peak 2 h after LPS inhalation. The influx of neutrophil into BALF increased gradually and reached a peak 24 h after LPS inhalation. After the inhalation of LPS, LTD4 and TNF contents in BALF increased within the first 2 h after LPS inhalation. However, other mediators were not detected or increased 6 h after LPS inhalation. Aeroinhalation of LTD4 and murine recombinant TNF-alpha caused airway hyperresponsiveness in guinea pigs. In addition, a LTD4 antagonist, BAYx7195, and an inhibitor of TNF, pentoxifylline, inhibited the LPS-induced airway hyperresponsiveness. These results suggest that LTs and/or TNF play an important role in the onset of airway hyperresponsiveness in guinea pigs.

Participation of Leukotriene D4 and Tumor Necrosis Factor on Lipopolysaccharide-induced Airway Hyperresponsiveness in Guinea Pigs.

Effect of Byakko-ka-ninjin-to on Experimental Allergic Cutaneous Reaction.

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Participation of Leukotriene D4 and Tumor Necrosis Factor on Lipopolysaccharide-induced Airway Hyperresponsiveness in Guinea Pigs.

Effect of Byakko-ka-ninjin-to on Experimental Allergic Cutaneous Reaction.