House dust mite‐driven neutrophilic airway inflammation in mice with TNFAIP3‐deficient myeloid cells is IL‐17‐independent

Vroman, Heleen; Das, Tridib; Bergen, Ingrid M.; Hulst, Jennifer A C van; Ahmadi, Fatemeh; Loo, Geert; Lubberts, Erik; Hendriks, Rudi W.; Kool, Mirjam

doi:10.1111/cea.13262

Cited by 7 publications

(4 citation statements)

References 53 publications

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Section: Discussionmentioning

confidence: 99%

“…Several studies have shown that IL-17 contributes to the development of airway inflammation and AHR in wild-type mice ( 45 – 48 ). Reported IL-17 levels were elevated in homogenized lung tissue; however, the values were not corrected for total protein in these studies ( 45 – 48 ). We reported previously that IL-17 was present in saline and HDME wild-type groups, and the levels were elevated in Arg2 -deficient mice ( 27 ).…”

Section: Discussionmentioning

confidence: 99%

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Barrier Housing and Gender Effects on Allergic Airway Disease in a Murine House Dust Mite Model

et al. 2021

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Allergic airway disease models use laboratory mice housed in highly controlled and hygienic environments, which provide a barrier between the mice and a predetermined list of specific pathogens excluded from the facility. In this study, we hypothesized that differences in facility barrier level and, consequently, the hygienic quality of the environment that mice inhabit impact the severity of pulmonary inflammation and lung function. Allergen-naive animals housed in the cleaner, high barrier (HB) specific pathogen-free facility had increased levels of inflammatory cytokines and higher infiltration of immune cells in the lung tissue but not in the bronchoalveolar lavage compared with mice housed in the less hygienic, low barrier specific pathogen-free facility. In both genders, house dust mite–induced airway disease was more severe in the HB than the low barrier facility. Within each barrier facility, female mice developed the most severe inflammation. However, allergen-naive male mice had worse lung function, regardless of the housing environment, and in the HB, the lung function in female mice was higher in the house dust mite model. Severe disease in the HB was associated with reduced lung microbiome diversity. The lung microbiome was altered across housing barriers, gender, and allergen-exposed groups. Thus, the housing barrier level impacts microbial-driven disease and gender phenotypes in allergic asthma. The housing of laboratory mice in more clean HB facilities aggravates lung immunity and causes a more severe allergic lung disease. ImmunoHorizons , 2021, 5: 33–47.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Barrier Housing and Gender Effects on Allergic Airway Disease in a Murine House Dust Mite Model

et al. 2021

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“…Newborns with asthma at school age had reduced A20 expression at birth, suggesting A20 as a possible biomarker predicting subsequent asthma [ 10 ]. A20 can also regulate T helper 2-mediated eosinophilic and neutrophilic airway inflammation via pulmonary conventional type 1 Langerin-expressing dendritic cells and myeloid cells, respectively [ 9 , 20 ].…”

Section: Discussionmentioning

confidence: 99%

Decreased ubiquitin modifying enzyme A20 associated with hyper-responsiveness to ovalbumin challenge following intrauterine growth restriction

Zheng

et al. 2023

Respir Res

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Background Intrauterine growth restriction (IUGR) is strongly correlated with an increased risk of asthma later in life. Farm dust protects mice from developing house dust mite-induced asthma, and loss of ubiquitin modifying enzyme A20 in lung epithelium would abolish this protective effect. However, the mechanisms of A20 in the development of asthma following IUGR remains unknown. Methods An IUGR rat model induced by maternal nutrient restriction was used for investigating the role of A20 in the response characteristics of IUGR rats to ovalbumin (OVA) challenge. The ubiquitination of proteins and N6-methyladenosine (m6A) modifications were used to further assess the potential mechanism of A20. Results IUGR can reduce the expression of A20 protein in lung tissue of newborn rats and continue until 10 weeks after birth. OVA challenging can increase the expression of A20 protein in lung tissue of IUGR rats, but its level was still significantly lower than the control OVA group. The differentially ubiquitinated proteins in lung tissues were also observed in IUGR and normal newborn rats. Furthermore, this ubiquitination phenomenon continued from the newborn to adulthood. In the detected RNA methylations, m6A abundance of the motif GGACA was the highest. The higher abundances of m6A modification of A20 mRNA from IUGR were negatively correlated with the trend of A20 protein levels. Conclusion These findings indicate A20 as a key regulator during the development of asthma following IUGR, providing further insight into the prevention of asthma induced by environmental factors.

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“…Previous mechanistic‐based studies have revealed a role for ubiquitin‐modifying enzyme TNFAIP3 (TNFa‐induced protein 3, also known as A20) in the modulation of CD4+ IL‐17+ T cells and myeloid cell–driven pulmonary neutrophil inflammation . TNFAIP3 expression in DCs is required for house dust mite (HDM)–specific TH17 cell differentiation through expression of the Th17‐instructing cytokines IL‐1β, IL‐6 and IL‐2314.…”

Section: Experimental Models Of Allergic Diseasementioning

confidence: 99%

Developments in the mechanisms of allergy in 2018 through the eyes of Clinical and Experimental Allergy, Part I

Roberts

Almqvist

Boyle

et al. 2019

Clin Experimental Allergy

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House dust mite‐driven neutrophilic airway inflammation in mice with TNFAIP3‐deficient myeloid cells is IL‐17‐independent

Cited by 7 publications

References 53 publications

Barrier Housing and Gender Effects on Allergic Airway Disease in a Murine House Dust Mite Model

Barrier Housing and Gender Effects on Allergic Airway Disease in a Murine House Dust Mite Model

Decreased ubiquitin modifying enzyme A20 associated with hyper-responsiveness to ovalbumin challenge following intrauterine growth restriction

Developments in the mechanisms of allergy in 2018 through the eyes of Clinical and Experimental Allergy, Part I

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