Endotoxin-stimulated innate immunity: A contributing factor for asthma

Reed, Charles E.; Milton, Donald K.

doi:10.1067/mai.2001.116862

Cited by 189 publications

(145 citation statements)

References 165 publications

Supporting

Mentioning

138

Contrasting

Unclassified

Order By: Relevance

“…Thus, our results and those described above indicate that the effect of LPS on allergic responses may vary according to dose, timing, and route of administration. It is possible that the detrimental effects of LPS on asthma may be related to the increased severity of the airway inflammation or to increased susceptibility to rhinovirus-induced colds that may result in chronic bronchitis and emphysema with development of irreversible airway obstruction (10).…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Bacterial Lipopolysaccharide Signaling Through Toll-Like Receptor 4 Suppresses Asthma-Like Responses Via Nitric Oxide Synthase 2 Activity

Rodríguez

Keller

Faquim-Mauro

et al. 2003

The Journal of Immunology

152

153

View full text Add to dashboard Cite

Asthma results from an intrapulmonary allergen-driven Th2 response and is characterized by intermittent airway obstruction, airway hyperreactivity, and airway inflammation. An inverse association between allergic asthma and microbial infections has been observed. Microbial infections could prevent allergic responses by inducing the secretion of the type 1 cytokines, IL-12 and IFN-γ. In this study, we examined whether administration of bacterial LPS, a prototypic bacterial product that activates innate immune cells via the Toll-like receptor 4 (TLR4) could suppress early and late allergic responses in a murine model of asthma. We report that LPS administration suppresses the IgE-mediated and mast cell-dependent passive cutaneous anaphylaxis, pulmonary inflammation, airway eosinophilia, mucus production, and airway hyperactivity. The suppression of asthma-like responses was not due to Th1 shift as it persisted in IL-12−/− or IFN-γ−/− mice. However, the suppressive effect of LPS was not observed in TLR4- or NO synthase 2-deficient mice. Our findings demonstrate, for the first time, that LPS suppresses Th2 responses in vivo via the TLR4-dependent pathway that triggers NO synthase 2 activity.

show abstract

Section: Discussionmentioning

confidence: 99%

“…It has been shown that exposure to airborne LPS can either protect against asthma or exacerbate it (reviewed in Ref. 10). The beneficial effects of LPS are thought to be mediated by enhanced secretion of the type 1 cytokines IL-12 and IFN-␥ that are known to down-modulate allergic responses (11,12).…”

mentioning

confidence: 99%

Bacterial Lipopolysaccharide Signaling Through Toll-Like Receptor 4 Suppresses Asthma-Like Responses Via Nitric Oxide Synthase 2 Activity

Rodríguez

Keller

Faquim-Mauro

et al. 2003

The Journal of Immunology

152

153

View full text Add to dashboard Cite

show abstract

“…5 Bacterial endotoxins, or lipopolysaccharides (LPS), which are ubiquitous in domestic and work environments, are known to induce airflow obstruction and bronchial hyperresponsiveness by inhalation. 6 Lipopolysaccharides alone can contribute to activation of airway neutrophils, which secrete inflammatory cytokines, including interleukin-8 (IL-8, CXCL-8) or myeloperoxidase (MPO). 7 Additionally, several studies have demonstrated that endotoxins affect the process of Th2 priming and augment inflammatory responses to allergen exposure.…”

Section: Introductionmentioning

confidence: 99%

Effect of Toll-like receptor 4 gene polymorphisms on work-related respiratory symptoms and sensitization to wheat flour in bakery workers

Cho

Kim

et al. 2011

Annals of Allergy, Asthma & Immunology

View full text Add to dashboard Cite

“…[1][2][3][4][5] Acquired immune responses in asthma are well characterised and involve allergen-induced T helper type 2 lymphocyte activation and consequent eosinophilic airway inflammation. Activated eosinophils release potent cytotoxic granules such as major basic protein and eosinophil cationic protein which induce airway hyper-responsiveness (AHR) and symptoms.…”

mentioning

confidence: 99%

Innate immune activation in neutrophilic asthma and bronchiectasis

Simpson

Grissell

Douwes

et al. 2007

Thorax

294

288

View full text Add to dashboard Cite

Background: The role of the innate immune system in the pathogenesis of asthma is unclear. Activation of innate immune receptors in response to bacterial lipopolysaccharide, viral infection and particulate matter triggers a pre-programmed inflammatory response, which involves interleukin (IL)8 and neutrophil influx. The inflammatory response in asthma is heterogeneous. Aim: To test the hypothesis that innate immune activation may be a relevant inflammatory mechanism in neutrophilic asthma where IL8 levels are increased. Methods: Induced sputum was obtained from non-smoking adults with asthma (n = 49), healthy controls (n = 13) and a positive reference group with bronchiectasis (n = 9). Subjects with asthma were classified into inflammatory subtypes using induced sputum cell counts. Sputum was examined for mRNA expression of the innate immune receptors toll-like receptor (TLR)2, TLR4 and CD14, and inflammatory cytokines. A separate sputum portion was dispersed and the supernatant assayed for surfactant protein A, IL8, soluble CD14 and endotoxin. Results: Expression of innate immune receptors was increased in subjects with bronchiectasis and neutrophilic asthma compared with other asthma subtypes and controls. Increased expression of the receptors TLR2, TLR4 and CD14, as well as the pro-inflammatory cytokines IL8 and IL1b, was observed. Subjects with neutrophilic asthma had higher airway levels of endotoxin than the other groups studied. Conclusion: There is evidence of activation of the innate immune system in asthma which results in the production of pro-inflammatory cytokines and may contribute to the pathogenesis of neutrophilic asthma.

show abstract

Endotoxin-stimulated innate immunity: A contributing factor for asthma

Cited by 189 publications

References 165 publications

Bacterial Lipopolysaccharide Signaling Through Toll-Like Receptor 4 Suppresses Asthma-Like Responses Via Nitric Oxide Synthase 2 Activity

Bacterial Lipopolysaccharide Signaling Through Toll-Like Receptor 4 Suppresses Asthma-Like Responses Via Nitric Oxide Synthase 2 Activity

Effect of Toll-like receptor 4 gene polymorphisms on work-related respiratory symptoms and sensitization to wheat flour in bakery workers

Innate immune activation in neutrophilic asthma and bronchiectasis

Contact Info

Product

Resources

About