Airway Administration of<i>Escherichia coli</i>Endotoxin to Mice Induces Glucocorticosteroid-Resistant Bronchoconstriction and Vasopermeation

Lefort, Jean; Motreff, Laurence; Vargäftig, B. Boris

doi:10.1165/ajrcmb.24.3.4289

Cited by 71 publications

(73 citation statements)

References 21 publications

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“…administration of 50 g per mouse. The airway resistance was evaluated by wholebody plethysmography (8). Bronchoconstriction was investigated at several time points.…”

Section: Endotoxin Administration and Measurement Of Airway Resistancementioning

confidence: 99%

“…The majority of these pathologic features of human airway inflammation have also been observed in experimental lung injury models. In mice, aerogenic exposure to endotoxin or LPS, a major component of the outmost membrane of Gram-negative bacteria, induces pulmonary inflammation with recruitment and activation of macrophages and neutrophils in the airways, local TNF production, alveolar-capillary leak, and also a direct bronchoconstriction (8). TLR, and especially TLR4, plays a critical role in the response to LPS (9).…”

mentioning

confidence: 99%

“…Lungs are a complex compartmentalized organ with separate barriers, namely the alveolar-capillary barrier, the microvascular endothelium, and the alveolar epithelium. Systemic LPS administration induces neutrophil sequestration into the pulmonary microvasculature without passage into the lung tissues and bronchoalveolar space (12), whereas neutrophil recruitment upon aerogenic LPS exposure occurs in all airway compartments (8). The mechanisms of these responses are still poorly understood, and we analyzed the role of TLR signaling and the contribution of different cell types in response to aerogenic LPS.…”

mentioning

confidence: 99%

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Both Hemopoietic and Resident Cells Are Required for MyD88-Dependent Pulmonary Inflammatory Response to Inhaled Endotoxin

Noulin

Quesniaux

Schnyder‐Candrian

et al. 2005

The Journal of Immunology

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Inhaled endotoxin induces an inflammatory response that contributes to the development and severity of asthma and other forms of airway disease. Here, we show that inhaled endotoxin-induced acute bronchoconstriction, TNF, IL-12p40, and KC production, protein leak, and neutrophil recruitment in the lung are abrogated in mice deficient for the adaptor molecule MyD88. Bronchoconstriction, inflammation, and protein leak are normal in Toll/IL-1R domain-containing adaptor inducing IFN-β-deficient mice. MyD88 is involved in TLR, but also in IL-1R-associated kinase 1-mediated IL-1R and -18R signaling. We exclude a role for IL-1 and IL-18 pathways in this response, as IL-1R1 and caspase-1 (ICE)-deficient mice develop lung inflammation while TLR4-deficient mice are unresponsive to inhaled LPS. Significantly, using bone marrow chimera, we demonstrate that both hemopoietic and resident cells are necessary for a full MyD88-dependent response to inhaled endotoxin; bronchoconstriction depends on resident cells while cytokine secretion is mediated by hemopoietic cells.

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“…administration of 50 g per mouse. The airway resistance was evaluated by wholebody plethysmography (8). Bronchoconstriction was investigated at several time points.…”

Section: Endotoxin Administration and Measurement Of Airway Resistancementioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Both Hemopoietic and Resident Cells Are Required for MyD88-Dependent Pulmonary Inflammatory Response to Inhaled Endotoxin

Noulin

Quesniaux

Schnyder‐Candrian

et al. 2005

The Journal of Immunology

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“…This phenomenon has been modelled in recent in vivo mouse models [25][26][27]. From these models, it emerges that the lipopolysaccharide (LPS)-mediated effects are largely regulated by the endogenous production of TNF.…”

Section: Natural Killer Cellsmentioning

confidence: 99%

Murine models of asthma

Kips¹,

Anderson²,

Fredberg³

et al. 2003

Eur Respir J

183

123

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In vivo animal models can offer valuable information on several aspects of asthma pathogenesis and treatment. The mouse is increasingly used in these models, mainly because this species allows for the application in vivo of a broad range of immunological tools, including gene deletion technology. Mice, therefore, seem particularly useful to further elucidate factors influencing the response to inhaled allergens. Examples include: the role of immunoregulatory mechanisms that protect against T-helper cell type 2 cell development; the trafficking of T-cells; and the contribution of the innate immunity. However, as for other animal species, murine models also have limitations. Mice do not spontaneously develop asthma and no model mimics the entire asthma phenotype. Instead, mice should be used to model specific traits of the human disease. The present task force report draws attention to specific aspects of lung structure and function that need to be borne in mind when developing such models and interpreting the results. In particular, efforts should be made to develop models that mimic the lung function changes characteristic of asthma as closely as possible. A large section of this report is therefore devoted to an overview of airway function and its measurement in mice.

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“…2009. 39: 1587-1596 DOI 10.1002 Innate immunity 1587 function and bronchoconstriction, cytokine and chemokine production, PMN recruitment, increased permeability of the alveolar epithelium and the associated endothelium [3][4][5][6]. TLR4 [7], together with MD-2, LPS-binding protein and CD14 detect endotoxins and play a critical role in the initiation of the pulmonary response to systemic and mucosal endotoxin administration [5,[8][9][10].…”

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confidence: 99%

Radioresistant cells expressing TLR5 control the respiratory epithelium's innate immune responses to flagellin

et al. 2009

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Bacterial products (such as endotoxins and flagellin) trigger innate immune responses through TLRs. Flagellin-induced signalling involves TLR5 and MyD88 and, according to some reports, TLR4. Whereas epithelial and dendritic cells are stimulated by flagellin in vitro, the cell contribution to the in vivo response is still unclear. Here, we studied the respective roles of radioresistant and radiosensitive cells in flagellin-induced airway inflammation in mice. We found that i.n. delivery of flagellin elicits a transient change in respiratory function and an acute, pro-inflammatory response in the lungs, characterized by TLR5-and MyD88-dependent chemokine secretion and neutrophil recruitment. In contrast, TLR4, CD14 and TRIF were not essential for flagellin-mediated responses, indicating that TLR4 does not cooperate with TLR5 in the lungs. Respiratory function, chemokine secretion and airway infiltration by neutrophils were dependent on radioresistant, TLR5-expressing cells. Furthermore, lung haematopoietic cells also responded to flagellin by activating TNF-a production. We suggest that the radioresistant lung epithelial cells are essential for initiating early, TLR5-dependent signalling in response to flagellin and thus triggering the lung's innate immune responses.Key words: Chemokine . Epithelium . Flagellin . Lung inflammation . TLR5 IntroductionUpon challenge with respiratory pathogens, the airways rapidly develop a pro-inflammatory response initiated by environmental agents including microbe-associated molecular patterns such as Gram-negative bacteria LPS or endotoxins. This proinflammatory reaction plays an important role in the innate defense against respiratory pathogens [1,2]. Physiological changes induced by endotoxin inhalation include pulmonary Ã These authors contributed equally to this work. Eur. J. Immunol. 2009. 39: 1587-1596 DOI 10.1002 Innate immunity 1587 function and bronchoconstriction, cytokine and chemokine production, PMN recruitment, increased permeability of the alveolar epithelium and the associated endothelium [3][4][5][6]. TLR4 [7], together with MD-2, LPS-binding protein and CD14 detect endotoxins and play a critical role in the initiation of the pulmonary response to systemic and mucosal endotoxin administration [5,[8][9][10]. The pulmonary inflammation to endotoxin involves TLR4 signalling in both the parenchyma cells like endothelial and epithelial cells and the haematopoietic cells, i.e. monocytes, dendritic cells and neutrophils [11]. In addition, TLR4 signalling contributes to the development and progression of chronic respiratory disease including asthma [12][13][14][15][16].Flagellin is the major constituent of flagella from Gramnegative and Gram-positive bacteria. TLR5 has been identified as the main pattern recognition receptor required for flagellinmediated immune signalling [17]. TLR5 signalling depends on MyD88 and results in activation of MAPK, nuclear translocation of NF-kB and production of various pro-inflammatory cytokines and chemokines [18]. Moreover, a previous ...

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Airway Administration ofEscherichia coliEndotoxin to Mice Induces Glucocorticosteroid-Resistant Bronchoconstriction and Vasopermeation

Cited by 71 publications

References 21 publications

Both Hemopoietic and Resident Cells Are Required for MyD88-Dependent Pulmonary Inflammatory Response to Inhaled Endotoxin

Both Hemopoietic and Resident Cells Are Required for MyD88-Dependent Pulmonary Inflammatory Response to Inhaled Endotoxin

Murine models of asthma

Radioresistant cells expressing TLR5 control the respiratory epithelium's innate immune responses to flagellin

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