scholarly journals Role of house-dust mites in childhood asthma

1974 ◽  
Vol 49 (9) ◽  
pp. 711-715 ◽  
Author(s):  
J. K. Sarsfield
Keyword(s):  
House Dust ◽  
Childhood Asthma ◽  
House Dust Mites ◽  
Dust Mites

scholarly journals Group 10 Allergens (Tropomyosins) from House-Dust Mites May Cause Covariation of Sensitization to Allergens from Other Invertebrates

2012 ◽  
Vol 3 (2) ◽  
pp. ar.2012.3.0036 ◽  
Author(s):  
Rubaba Hamid Shafique ◽  
Muhammad Inam ◽  
Muhammad Ismail ◽  
Farhana Riaz Chaudhary
Keyword(s):  
House Dust ◽  
Cross Reactivity ◽  
Amino Acid Sequences ◽  
House Dust Mites ◽  
Published Data ◽  
Dust Mites ◽  
Cockroach Allergen ◽  
Ige Binding ◽  
Group 10

Group 10 allergens (tropomyosins) have been assumed to be a major cause of cross-reactivity between house-dust mites (HDMs) and other invertebrates. Despite all of the published data regarding the epidemiology, percent IgE binding and level of sensitization in the population, the role of tropomyosin as a cross-reactive allergen in patients with multiple allergy syndrome still remains to be elucidated. Homology between amino acid sequences reported in allergen databases of selected invertebrate tropomyosins was determined with Der f 10 as the reference allergen. The 66.9 and 54.4% identities were found with selected crustacean and insect species, respectively, whereas only 20.4% identity was seen with mollusks. A similar analysis was performed using reported B-cell IgE-binding epitopes from Met e1 (shrimp allergen) and Bla g7 (cockroach allergen) with other invertebrate tropomyosins. The percent identity in linear sequences was higher than 35% in mites, crustaceans, and cockroaches. The polar and hydrophobic regions in these groups were highly conserved. These findings suggest that tropomyosin may be a major cause of covariation of sensitization between HDMs, crustaceans, and some species of insects and mollusks.

scholarly journals ROLE OF HOUSE DUST MITES IN KAWASAKI SYNDROME (KS)

1984 ◽  
Vol 18 ◽  
pp. 275A-275A
Author(s):  
Mary P Glode ◽  
Jane C Burns ◽  
Lynn Joffe ◽  
Larry Arlian ◽  
Alan Adinoff ◽  
...  
Keyword(s):  
House Dust ◽  
House Dust Mites ◽  
Kawasaki Syndrome ◽  
Dust Mites

scholarly journals Caspase-11 regulates lung inflammation in response to house dust mites

2020 ◽  
Author(s):  
Arwa Abu khweek ◽  
Marisa R. Joldrichsen ◽  
Eunsoo Kim ◽  
Zayed Attia ◽  
Kathrin Krause ◽  
...  
Keyword(s):  
House Dust ◽  
Inflammatory Responses ◽  
Allergic Sensitization ◽  
Allergic Inflammation ◽  
House Dust Mites ◽  
Host Responses ◽  
Dust Mites ◽  
Molecular Patterns

Abstract Asthma is an inflammatory lung disorder characterized by mucus hypersecretion, cellular infiltration, and bronchial hyper-responsiveness. House dust mites (HDM) are the most prevalent cause of allergic sensitization. Canonical and noncanonical inflammasomes are multiprotein complexes that assemble in response to pathogen or danger-associated molecular patterns (PAMPs or DAMPs). Murine caspase-11 engages the noncanonical inflammasome. We addressed the role of caspase-11 in mediating host responses to HDM and subsequent allergic inflammation using caspase-11−/− mice, which lack caspase-11 while express caspase-1. We found that HDM induce caspase-11 expression in vitro. The presence of IL-4 and IL-13 promotes caspase-11 expression. Additionally, caspase-11−/− macrophages show reduced release of (KC, IL-6 and IL-12) cytokines, and express lower levels of costimulatory molecules (e.g., CD40, CD86 and MHCII) in response to HDM stimulation. Notably, HDM sensitization of caspase-11−/− mice resulted in similar levels of IgE responses and hypothermia in response to nasal HDM challenge compared to WT. However, analysis of cell numbers and cytokines in bronchiolar alveolar fluid (BALF), as well as histological lung tissue showed altered inflammatory responses and reduced neutrophilia in the airways of the caspase-11−/− mice. These findings indicate that caspase-11 regulates airway inflammation in response to HDM exposure.

scholarly journals Current view on studying of the role of tropomyiosin in the development of crossallergic reactions

2018 ◽  
Vol 15 (3) ◽  
pp. 16-24
Author(s):  
T G Fedoskova ◽  
A I Martynov ◽  
N V Kobizskaya ◽  
D V Shabanov
Keyword(s):  
House Dust ◽  
Preventive Measures ◽  
Clinical Symptoms ◽  
Cross Reactivity ◽  
House Dust Mites ◽  
Current View ◽  
Allergic Reactions ◽  
Dust Mites ◽  
High Prevalence

Cross-reactivity to proteins is the issue of the day due to the severity of clinical symptoms, high prevalence of this phenomenon and the absence of preventive measures . Cross-reactivity is found in pollen, house dust, insects, food allergy, helminthes etc. Multiple studies have confirmed the important role of the protein tropomyosin in the development of sensitization to house dust mites allergens, food allergens and insects. The presence of tropomyosin is detected in the allergen spectrum of many arthropods, in particular insects and crustaceans. The researchers have noted the possibility of development of various cross-allergic reactions to tropomyosin protein. Arthropods are the main type of the Earth’s fauna. Clinical symptoms of allergic reactions to Arthropods differ in severity; this is the issue of studying of the the cross-reactivity to tropomyosin protein.

scholarly journals Lung eosinophilia induced by house dust mites or ovalbumin is modulated by nicotinic receptor α7 and inhibited by cigarette smoke

2018 ◽  
Vol 315 (4) ◽  
pp. L553-L562 ◽  
Author(s):  
Lorise C. Gahring ◽  
Elizabeth J. Myers ◽  
Diane M. Dunn ◽  
Robert B. Weiss ◽  
Scott W. Rogers
Keyword(s):  
House Dust ◽  
Nicotinic Receptor ◽  
Inflammatory Responses ◽  
Adverse Outcomes ◽  
House Dust Mites ◽  
Dust Mites ◽  
Lung Eosinophilia ◽  
A Cell

Eosinophilia (EOS) is an important component of airway inflammation and hyperresponsiveness in allergic reactions including those leading to asthma. Although cigarette smoking (CS) is a significant contributor to long-term adverse outcomes in these lung disorders, there are also the curious reports of its ability to produce acute suppression of inflammatory responses including EOS through poorly understood mechanisms. One possibility is that proinflammatory processes are suppressed by nicotine in CS acting through nicotinic receptor α7 (α7). Here we addressed the role of α7 in modulating EOS with two mouse models of an allergic response: house dust mites (HDM; Dermatophagoides sp.) and ovalbumin (OVA). The influence of α7 on EOS was experimentally resolved in wild-type mice or in mice in which a point mutation of the α7 receptor (α7E260A:G) selectively restricts normal signaling of cellular responses. RNA analysis of alveolar macrophages and the distal lung epithelium indicates that normal α7 function robustly impacts gene expression in the epithelium to HDM and OVA but to different degrees. Notable was allergen-specific α7 modulation of Ccl11 and Ccl24 (eotaxins) expression, which was enhanced in HDM but suppressed in OVA EOS. CS suppressed EOS induced by both OVA and HDM, as well as the inflammatory genes involved, regardless of α7 genotype. These results suggest that EOS in response to HDM or OVA is through signaling pathways that are modulated in a cell-specific manner by α7 and are distinct from CS suppression.

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