scholarly journals Laboratory mice with a wild microbiota generate strong allergic immune responses

2021 ◽  
Author(s):  
Junjie Ma ◽  
Cajsa H Classon ◽  
Julian M Stark ◽  
Muzhen Li ◽  
Huey-Jy Huang ◽  
...  
Keyword(s):  
Immune Responses ◽  
Allergic Inflammation ◽  
Hygiene Hypothesis ◽  
House Dust Mites ◽  
Dust Mites ◽  
Laboratory Mice ◽  
Pathogenic Potential ◽  
Peptide Antigens ◽  
Cell Responses ◽  
Allergic Disorders

Allergic disorders are caused by a combination of hereditary and environmental factors. The hygiene hypothesis postulates that early life microbial exposures impede the development of subsequent allergic disease. However, unambiguous evidence that microbes reduce the development of allergic disorders is still lacking. Recently developed wildling mice contain a rich and diverse commensal and encounter a repertoire of microbes typical of the wild, with pathogenic potential. Here, we probed the hygiene hypothesis by comparing the development of allergic inflammation in wildlings to that of genetically identical mice lacking diverse microbial exposure. We find that wildlings develop stronger allergic inflammation in response to house dust mites with allergic T cell responses driven not only by cognate peptide antigens, but also by innate cytokines. In all, the results suggest that high microbial content and diversity potentiates, rather than restricts, allergic immune responses.

scholarly journals AMCase is a crucial regulator of type 2 immune responses to inhaled house dust mites

2015 ◽  
Vol 112 (22) ◽  
pp. E2891-E2899 ◽  
Author(s):  
Lark Kyun Kim ◽  
Rimpei Morita ◽  
Yasushi Kobayashi ◽  
Stephanie C. Eisenbarth ◽  
Chun Geun Lee ◽  
...  
Keyword(s):  
Immune Responses ◽  
House Dust ◽  
House Dust Mites ◽  
Mouse Lung ◽  
Dust Mites ◽  
Dust Mite ◽  
Caspase 7 ◽  
Acidic Mammalian Chitinase ◽  
Subsequent Activation

Chitinases are enzymes that cleave chitin, a component of the exoskeleton of many organisms including the house dust mite (HDM). Here we show that knockin mice expressing an enzymatically inactive acidic mammalian chitinase (AMCase), the dominant true chitinase in mouse lung, showed enhanced type 2 immune responses to inhaled HDM. We found that uncleaved chitin promoted the release of IL-33, whereas cleaved chitin could be phagocytosed and could induce the activation of caspase-1 and subsequent activation of caspase-7; this results in the resolution of type 2 immune responses, probably by promoting the inactivation of IL-33. These data suggest that AMCase is a crucial regulator of type 2 immune responses to inhaled chitin-containing aeroallergens.

Low-level exposure to house dust mites stimulates T-cell responses during early childhood independent of atopy

1996 ◽  
Vol 26 (7) ◽  
pp. 775-779 ◽  
Author(s):  
B. Bjorksten ◽  
B. J. Holt ◽  
M. J. Baron-Hay ◽  
A. K. M. Munir ◽  
P. G. Holt
Keyword(s):  
Early Childhood ◽  
T Cell ◽  
House Dust ◽  
T Cell Responses ◽  
House Dust Mites ◽  
Dust Mites ◽  
Low Level ◽  
Cell Responses

Low-level exposure to house dust mites stimulates T-cell responses during early childhood independent of atopy

1996 ◽  
Vol 26 (7) ◽  
pp. 775-779 ◽  
Author(s):  
B. BJÖRKSTÉN ◽  
B. J. HOLT ◽  
M. J. BARON-HAY ◽  
A. K. M. MUNIR ◽  
P. G. HOLT
Keyword(s):  
Early Childhood ◽  
T Cell ◽  
House Dust ◽  
T Cell Responses ◽  
House Dust Mites ◽  
Dust Mites ◽  
Low Level ◽  
Cell Responses

Epicutaneous sensitization with house dust mites leads to pulmonary immune responses in dogs

2002 ◽  
Vol 109 (1) ◽  
pp. S35-S35
Author(s):  
Edward G Barrett ◽  
Karin Rudolph ◽  
Shan-Ze Wang ◽  
Bruce A Muggenburg ◽  
Monique Nysus ◽  
...  
Keyword(s):  
Immune Responses ◽  
House Dust ◽  
House Dust Mites ◽  
Dust Mites ◽  
Epicutaneous Sensitization

Asma infantil: Efectos inmunomoduladores de los liofilizados bacterianos

2021 ◽  
pp. 1-2
Author(s):  
Patricia Ximena Solari
Keyword(s):  
T Lymphocytes ◽  
Immune Responses ◽  
Allergic Asthma ◽  
Respiratory Infections ◽  
Trial Registration ◽  
House Dust Mites ◽  
Dust Mites ◽  
Bacterial Lysate ◽  
Clinical Trial Registration ◽  
Registry Record

Background: Polyvalent Mechanical Bacterial Lysate (PMBL®) contains antigens of bacteria responsible for respiratory infections. PMBL® has been proven to reduce the number of respiratory infections, and in its use, immunological benefits have been seen in allergic patients. PMBL® activates both innate and specific immune responses. The lysate induces dendritic cells, T and B lymphocytes and IgA secretion, as well as the production of antibodies directed against administered bacterial antigens. Moreover, it increases the response against other bacteria and viruses. The immunologic mechanism of lysate’s action is not yet clearly determined. The objective of this study was to assess the effect of PMBL® on T cells in children with allergic asthma. Methods: This study was a part of the EOLIA study. Herein, 49 children with allergic asthma and house dust mites allergy were included: 21 in PMBL® and 28 in the Placebo group, both, drug and placebo were administered sublingually. The tests were done at baseline and 12 weeks after the last tablet intake. The lymphocytes CD45+, lymphocytes T CD3+, CD3+CD25+, CD3+CD69+, Th CD3+CD4+, CD4+CD25+, CD4+CD25+ high, CD4+CD69+, Treg CD4+CD25+FOXP3, Tc CD3+CD8+, CD8+CD25+, CD8+CD69+, NK-like T CD3+CD16+CD56+ and NK cells CD3−CD16+CD56+ were described. Results: At baseline, no significant differences between groups relative to blood count cells were observed, except for eosinophils. After 12 weeks, we observed an increase of T lymphocytes count. In addition, CD4+CD25+FOXP3+, CD8+ and CD3−CD16+CD56+ and (insignificantly) Th count increased. However, CD69+ and CD25+ subset of CD3+ significantly decreased. Conclusions: The EOLIA study demonstrated that PMBL® administration 10 days per month for 3 months changed the panel of T lymphocytes. Trial registration Clinical Trial Registration: This study was a part of the EOLIA (Efficacy Of mechanical bacterial Lysate In Allergic children), a clinical study NCT02541331. Frederic Durmont, MD Lallemand Pharma International AG. Date of registration 09/08/2013. URL of trial registry record: https://clinicaltrials.gov/ct2/show/study/NCT02541331.

scholarly journals A major house dust mite allergen disrupts the immunoglobulin E network by selectively cleaving CD23: innate protection by antiproteases.

1995 ◽  
Vol 182 (5) ◽  
pp. 1537-1544 ◽  
Author(s):  
C R Hewitt ◽  
A P Brown ◽  
B J Hart ◽  
D I Pritchard
Keyword(s):  
Cell Surface ◽  
Immune Responses ◽  
Allergic Asthma ◽  
House Dust ◽  
House Dust Mite ◽  
Immunoglobulin E ◽  
House Dust Mites ◽  
Dust Mites ◽  
Group I ◽  
Dust Mite

Asthma is a chronic life-threatening disease of worldwide importance. Although allergic asthma and related atopic conditions correlate strongly with immune sensitization to house dust mites, it is unclear why antigens from mites provoke such powerful allergic immune responses. We have characterized the protease activity of Der p I, the group I protease allergen of the house dust mite Dermatophagoides pteronyssinus, and here report that it cleaves the low-affinity immunoglobulin (Ig) E Fc receptor (CD23) from the surface of human B lymphocytes. Der p I selectively cleaves CD23 and has no effect on the expression of any other B cell surface molecules tested. We speculate that this loss of cell surface CD23 from IgE-secreting B cells may promote and enhance IgE immune responses by ablating an important feedback inhibitory mechanism that normally limits IgE synthesis. Furthermore, since soluble CD23 is reported to promote IgE production, fragments of CD23 released by Der p I may directly enhance the synthesis of IgE. alpha 1-Antiprotease, a pulmonary antiprotease, is also shown to inhibit the cleavage of CD23 by Der p I. This may be significant in the etiopathogenesis of asthma, because other indoor pollutants associated with asthma are known to potently inhibit this antiprotease. These data suggest that the proteolytic activity of Der p I, the group I allergen of the house dust mite D. pteronyssinus, is mechanistically linked to the potent allergenicity of house dust mites. Furthermore, inhibition of Der p I by alpha 1-antiprotease suggests a mechanism by which confounding factors, such as tobacco smoke, may act as a risk factor for allergic asthma.

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.

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