Endotoxin-Induced Airway Inflammation and Asthma Models

Helyes, Zsuzsanna; Hajna, Zsófia

doi:10.1007/978-1-62703-077-9_16

Cited by 5 publications

(5 citation statements)

References 183 publications

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“…In the animal experiments, 10-18-week-old female C57BL/6J mice [20] weighing 21.7 ± 0.30 g (mean ± SEM) at the beginning of the experiment were used. The age distribution of the mice was similar in each group to avoid age-related differences.…”

Section: Animalsmentioning

confidence: 99%

“…The endotoxin (lipopolysaccharide: LPS)-induced acute airway inflammation mouse model is the most frequently applied, well-reproducible mechanism model for the study of EOs in acute respiratory inflammation [4,[16][17][18][19]. LPS is a component of the Gram-negative bacterial cell wall, which induces interstitial pneumonitis and acute respiratory obstruction by a well-defined Toll-like receptor-4 activation on macrophages, resulting in the release of several inflammatory mediators and consequent neutrophil activation [20].…”

Section: Introductionmentioning

confidence: 99%

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Pinus sylvestris L. and Syzygium aromaticum (L.) Merr. & L. M. Perry Essential Oils Inhibit Endotoxin-Induced Airway Hyperreactivity despite Aggravated Inflammatory Mechanisms in Mice

et al. 2022

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Scots pine (SO) and clove (CO) essential oils (EOs) are commonly used by inhalation, and their main components are shown to reduce inflammatory mediator production. The aim of our research was to investigate the chemical composition of commercially available SO and CO by gas chromatography–mass spectrometry and study their effects on airway functions and inflammation in an acute pneumonitis mouse model. Inflammation was evoked by intratracheal endotoxin and EOs were inhaled three times during the 24 h experimental period. Respiratory function was analyzed by unrestrained whole-body plethysmography, lung inflammation by semiquantitative histopathological scoring, myeloperoxidase (MPO) activity and cytokine measurements. α-Pinene (39.4%) was the main component in SO, and eugenol (88.6%) in CO. Both SO and CO significantly reduced airway hyperresponsiveness, and prevented peak expiratory flow, tidal volume increases and perivascular edema formation. Meanwhile, inflammatory cell infiltration was not remarkably affected. In contrast, MPO activity and several inflammatory cytokines (IL-1β, KC, MCP-1, MIP-2, TNF-α) were aggravated by both EOs. This is the first evidence that SO and CO inhalation improve airway function, but enhance certain inflammatory parameters. These results suggest that these EOs should be used with caution in cases of inflammation-associated respiratory diseases.

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Section: Animalsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Pinus sylvestris L. and Syzygium aromaticum (L.) Merr. & L. M. Perry Essential Oils Inhibit Endotoxin-Induced Airway Hyperreactivity despite Aggravated Inflammatory Mechanisms in Mice

et al. 2022

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“…Via the p38-MAPK signaling pathway it induces the activation and accumulation of immune cells [91,92]. As a result, inflammatory cytokines and proinflammatory mediators (e.g., bradykinin, leukotrienes and prostaglandins) are released from the activated immune cells directly activating the sensory nerve endings [93]. Beside the activation of immune cells, LPS also elicits bronchial contraction in the lung causing enhanced airway resistance [94].…”

Section: Endotoxin-induced Acute Pneumonitismentioning

confidence: 99%

Complex Regulatory Role of the TRPA1 Receptor in Acute and Chronic Airway Inflammation Mouse Models

Hajna

Csekő

Kemény

et al. 2020

IJMS

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The Transient Receptor Potential Ankyrin 1 (TRPA1) cation channel expressed on capsaicin-sensitive afferents, immune and endothelial cells is activated by inflammatory mediators and exogenous irritants, e.g., endotoxins, nicotine, crotonaldehyde and acrolein. We investigated its involvement in acute and chronic pulmonary inflammation using Trpa1 gene-deleted (Trpa1−/−) mice. Acute pneumonitis was evoked by intranasal Escherichia coli endotoxin (lipopolysaccharide: LPS) administration, chronic bronchitis by daily cigarette smoke exposure (CSE) for 4 months. Frequency, peak inspiratory/expiratory flows, minute ventilation determined by unrestrained whole-body plethysmography were significantly greater, while tidal volume, inspiratory/expiratory/relaxation times were smaller in Trpa1−/− mice. LPS-induced bronchial hyperreactivity, myeloperoxidase activity, frequency-decrease were significantly greater in Trpa1−/− mice. CSE significantly decreased tidal volume, minute ventilation, peak inspiratory/expiratory flows in wildtypes, but not in Trpa1−/− mice. CSE remarkably increased the mean linear intercept (histopathology), as an emphysema indicator after 2 months in wildtypes, but only after 4 months in Trpa1−/− mice. Semiquantitative histopathological scores were not different between strains in either models. TRPA1 has a complex role in basal airway function regulation and inflammatory mechanisms. It protects against LPS-induced acute pneumonitis and hyperresponsiveness, but is required for CSE-evoked emphysema and respiratory deterioration. Further research is needed to determine TRPA1 as a potential pharmacological target in the lung.

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“…In the animal experiments, 10-18 week old female C57BL/6J mice [22] were used weighing 20.8 ± 0.26 g (Mean ± SEM) at the beginning of the experiment (Table S1). In order to avoid age-related differences, the age distribution of the mice was similar in each group.…”

Section: Animalsmentioning

confidence: 99%

“…The endotoxin (lipopolysaccharide: LPS)-induced acute airway inflammation mouse model is the most commonly used, well-reproducible mechanism model for the study of EOs in acute respiratory inflammation [10,13,15,21]. LPS is a compound of the Gram-negative bacterial cell wall that causes interstitial pneumonitis and acute respiratory obstruction with a well-defined mechanism by activating Toll-like receptor-4 on macrophages, resulting in the release of several inflammatory mediators and consequent neutrophil activation after intranasal or intratracheal administration [22].…”

Section: Introductionmentioning

confidence: 99%

Effects of Thymus vulgaris L., Cinnamomum verum J.Presl and Cymbopogon nardus (L.) Rendle Essential Oils in the Endotoxin-induced Acute Airway Inflammation Mouse Model

et al. 2020

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Thyme (TO), cinnamon (CO), and Ceylon type lemongrass (LO) essential oils (EOs) are commonly used for inhalation. However, their effects and mechanisms on inflammatory processes are not well-documented, and the number of in vivo data that would be important to determine their potential benefits or risks is low. Therefore, we analyzed the chemical composition and investigated the activity of TO, CO, and LO on airway functions and inflammatory parameters in an acute pneumonitis mouse model. The components of commercially available EOs were measured by gas chromatography–mass spectrometry. Airway inflammation was induced by intratracheal endotoxin administration in mice. EOs were inhaled during the experiments. Airway function and hyperresponsiveness were determined by unrestrained whole-body plethysmography on conscious animals. Myeloperoxidase (MPO) activity was measured by spectrophotometry from lung tissue homogenates, from which semiquantitative histopathological scores were assessed. The main components of TO, CO, and LO were thymol, cinnamaldehyde, and citronellal, respectively. We provide here the first evidence that TO and CO reduce inflammatory airway hyperresponsiveness and certain cellular inflammatory parameters, so they can potentially be considered as adjuvant treatments in respiratory inflammatory conditions. In contrast, Ceylon type LO inhalation might have an irritant effect (e.g., increased airway hyperresponsiveness and MPO activity) on the inflamed airways, and therefore should be avoided.

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Endotoxin-Induced Airway Inflammation and Asthma Models

Cited by 5 publications

References 183 publications

Pinus sylvestris L. and Syzygium aromaticum (L.) Merr. & L. M. Perry Essential Oils Inhibit Endotoxin-Induced Airway Hyperreactivity despite Aggravated Inflammatory Mechanisms in Mice

Pinus sylvestris L. and Syzygium aromaticum (L.) Merr. & L. M. Perry Essential Oils Inhibit Endotoxin-Induced Airway Hyperreactivity despite Aggravated Inflammatory Mechanisms in Mice

Complex Regulatory Role of the TRPA1 Receptor in Acute and Chronic Airway Inflammation Mouse Models

Effects of Thymus vulgaris L., Cinnamomum verum J.Presl and Cymbopogon nardus (L.) Rendle Essential Oils in the Endotoxin-induced Acute Airway Inflammation Mouse Model

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