House dust mite induces direct airway inflammation<i>in vivo</i>: implications for future disease therapy?

Alba, Jorge De; Raemdonck, Kristof; Dekkak, Abdel; Collins, Michael; Wong, Sing‐Wai; Nials, Anthony T.; Knowles, Richard G.; Belvisi, Maria G.; Birrell, Mark A.

doi:10.1183/09031936.00022908

Cited by 46 publications

(41 citation statements)

References 42 publications

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“…Furthermore, the in vitro effects could not be prevented by heat inactivation and could not be mimicked by LPS administration. In line with our observations, De Alba et al have shown that the Greer extract was still able to induce manifestations of asthma upon heat inactivation in a rat model 26. Our data show for the first time that serine/cysteine proteases and chitinases in HDM extracts are not critically required for disruption of epithelial barrier function in vitro and innate immune responses in vivo, and hence subsequent allergic sensitisation and eosinophilic airway inflammation.…”

Section: Discussionsupporting

confidence: 92%

The composition of house dust mite is critical for mucosal barrier dysfunction and allergic sensitisation

Post

Nawijn

Hackett³

et al. 2011

Thorax

137

143

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Section: Discussionsupporting

confidence: 92%

The composition of house dust mite is critical for mucosal barrier dysfunction and allergic sensitisation

Post

Nawijn

Hackett³

et al. 2011

Thorax

137

143

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“…We used a clinically relevant murine model of asthma induced by repeated exposure to HDM (D. pteronyssinus), a common aeroallergen that is an environmental trigger and risk factor for the development of persistent asthma (14,24). HDM is a complex mixture of proteins and lipopolysaccharide, which can induce airway inflammation via allergic and nonallergic mechanisms (25)(26)(27). Furthermore, the mechanism of HDM-induced asthma, involves Toll-like receptor 4 signaling in airway epithelial cells, with resultant activation of innate and adaptive immune responses (28).…”

Section: Discussionmentioning

confidence: 99%

Apolipoprotein E Negatively Regulates House Dust Mite–induced Asthma via a Low-Density Lipoprotein Receptor–mediated Pathway

Yao

Fredriksson²,

Yu³

et al. 2010

Am J Respir Crit Care Med

115

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Rationale: Distinct sets of corticosteroid-unresponsive genes modulate disease severity in asthma. Objectives: To identify corticosteroid-unresponsive genes that provide new insights into disease pathogenesis and asthma therapeutics. Methods: Experimental murine asthma was induced by nasal administration of house dust mite for 5 days per week. Dexamethasone and apolipoprotein E (apo E) mimetic peptides were administered via osmotic minipumps. Measurements and Main Results: Genome-wide expression profiling of the lung transcriptome in a house dust mite-induced model of murine asthma identified increases in apo E mRNA levels that persisted despite corticosteroid treatment. House dust mite-challenged apo E 2/2 mice displayed enhanced airway hyperreactivity and goblet cell hyperplasia, which could be rescued by administration of an apo E(130-149) mimetic peptide. Administration of the apo E(130-149) mimetic peptide to house dust mite-challenged apo E 2/2 mice also inhibited eosinophilic airway inflammation, IgE production, and the expression of Th2 and Th17 cytokines. House dust mite-challenged low-density lipoprotein receptor (LDLR) knockout mice displayed a similar phenotype as apo E 2/2 mice with enhanced airway hyperreactivity, goblet cell hyperplasia, and mucin gene expression, but could not be rescued by the apo E(130-149) mimetic peptide, consistent with a LDLR-dependent mechanism. Conclusions: These findings for the first time identify an apo E-LDLR pathway as an endogenous negative regulator of airway hyperreactivity and goblet cell hyperplasia in asthma. Furthermore, our results demonstrate that strategies that activate the apo E-LDLR pathway, such as apo E mimetic peptides, might be developed into a novel treatment approach for patients with asthma.

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“…In the present study, we assessed sensitisation to house dust mites, cat fur and grass pollen, three common allergens with a high prevalence of sensitisation in our community. House dust mite (D. pteronyssinus) exposure is linked to increased cellular inflammation, including eosinophilia and an increased responsiveness or sensitivity to methacholine [7,8], and plays an important role in the initiation of allergic airway inflammation [9]. In this study, elevated IgE antibodies to D. pteronyssinus did not correlate with the occurrence of adverse respiratory events.…”

Section: Discussionmentioning

confidence: 64%

Peri-operative adverse respiratory events in children

et al. 2014

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SummaryThree quarters of all critical incidents and a third of all peri-operative cardiac arrests in paediatric anaesthesia are caused by adverse respiratory events. We screened for risk factors from children's and their families' histories, and assessed the usefulness of common markers of allergic sensitisation of the airway as surrogates for airway inflammation and increased risk for adverse respiratory events. One hundred children aged up to 16 years with two or more risk factors undergoing elective surgery were included in the study. Eosinophil counts, IgE level, specific IgE for D. pteronyssinus, cat epithelia and Gx2 (grass pollen) were measured for each child and adverse respiratory events (bronchospasm, laryngospasm, oxygen desaturation < 95%, severe persistent coughing, airway obstruction and postoperative stridor) were recorded. Twenty-one patients had an adverse respiratory event but allergic markers were poor predictors. Binary logistic regression showed a lack of predictive value of the eosinophil range and adverse respiratory events (p = 0.249). Receiver operating characteristic (ROC) curves for the presence of adverse respiratory events vs level of specific IgE antibody (to Gx2 (AUC 0.614), cat epithelia (0.564) and D. pteronyssinus (0.520)) demonstrated poor predictive values. However, the presence of risk factors was strongly associated with adverse respiratory events (p < 0.001) and a ROC-curve analysis indicated a fair capacity to predict adverse respiratory events (AUC 0.788). There was a significant difference (p = 0.001) between the presence of adverse respiratory events in patients with more than four (p = 0.006), compared with less than four (p = 0.001), risk factors. We conclude that while risk factors taken from the child's (or family) history proved good predictors of adverse respiratory events, immunological markers of allergic sensitisation demonstrated low predictive values. Pre-operative identification of children at high risk for an adverse respiratory event should rely on clinical, rather than immunological, assessment.

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House dust mite induces direct airway inflammationin vivo: implications for future disease therapy?

Cited by 46 publications

References 42 publications

The composition of house dust mite is critical for mucosal barrier dysfunction and allergic sensitisation

The composition of house dust mite is critical for mucosal barrier dysfunction and allergic sensitisation

Apolipoprotein E Negatively Regulates House Dust Mite–induced Asthma via a Low-Density Lipoprotein Receptor–mediated Pathway

Peri-operative adverse respiratory events in children

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