<scp>IL</scp>‐33 signalling contributes to pollutant‐induced allergic airway inflammation

Grove, Katrien C. De; Provoost, Sharen; Braun, Harald; Blomme, Evy; Teufelberger, Andrea Renate; Krysko, Olga; Beyaert, Rudi; Joos, Guy; Maes, Tania

doi:10.1111/cea.13261

Cited by 34 publications

(33 citation statements)

References 44 publications

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“…Our data further suggest that the absence of IL-33/ST2 signaling may hinder the role of OVA, which is also a contribution of Bb M-16V. Some studies have presented similar conclusions in other antigen-specific mouse models (De Grove et al, 2018;Teufelberger et al, 2018).…”

Section: Quantification and Statistical Analysissupporting

confidence: 83%

Bifidobacterium breve M‐16V alters the gut microbiota to alleviate OVA‐induced food allergy through IL‐33/ST2 signal pathway

Chen

et al. 2020

Journal Cellular Physiology

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There has been a marked increase in life‐threatening food allergy (FA). One hypothesis is that changes in bacterial communities may be key to FA. To better understand how gut microbiota regulates FA in humans, we established a mouse model with FA induced by ovalbumin. We found that the mice with FA had abnormal bacterial composition, accompanied by increased immunoglobulin G, immunoglobulin E, and interleukin‐4/interferon‐γ, and there existed a certain coherence between them. Interestingly, Bifidobacterium breve M‐16V may alter the gut microbiota to alleviate the allergy symptoms by IL‐33/ST2 signaling. Our results indicate that gut microbiota is essential for regulating FA to dietary antigens and demonstrate that intervention in bacterial community regulation may be therapeutically related to FA.

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Section: Quantification and Statistical Analysissupporting

confidence: 83%

Bifidobacterium breve M‐16V alters the gut microbiota to alleviate OVA‐induced food allergy through IL‐33/ST2 signal pathway

Chen

et al. 2020

Journal Cellular Physiology

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“…Only mice co-exposed to HDM + DEP demonstrated increased IL-33 lung levels, Th2 inflammation, and mild AHR. 22 Neutralizing IL-33, by administering soluble ST2 after each intranasal challenge, significantly decreased Th2 inflammation but not AHR. 22 Importantly, in our model, ST2-deficient BALB/c mice exposed to HDM + DEP demonstrate a 50% decrease in AHR, the most clinically relevant outcome in a mouse model of allergic airway disease.…”

Section: Discussionmentioning

confidence: 98%

“…22 Neutralizing IL-33, by administering soluble ST2 after each intranasal challenge, significantly decreased Th2 inflammation but not AHR. 22 Importantly, in our model, ST2-deficient BALB/c mice exposed to HDM + DEP demonstrate a 50% decrease in AHR, the most clinically relevant outcome in a mouse model of allergic airway disease. Further, the fact that both studies reach an overall similar conclusion, despite using different mouse strains, sources of DEP, challenge protocols and approaches to blocking IL33 signaling, strengthens both studies and strongly support a role for Innate cells such as ILC2, basophils, mast cells, and eosinophils constitutively express ST2 and have been shown to release Th2 cytokines upon IL33 stimulation.…”

Section: Discussionmentioning

confidence: 98%

“…De Grove et al observed a significant accumulation of ILC2 in the BALF of HDM + DEP challenged mice that was alleviate in ST2 −/− mice. 22 However, the contribution of ILC2 to DEP-induced exacerbation of allergic airway responses appears limited, as the same group previously demonstrated that mice lacking all ILCs (RORα fl/fl IL7R Cre C57Bl/6 mice) only showed partial decreases in Th2 inflammation following co-exposure to HDM and DEP. 28 Hence, ILC2s are unlikely to play a major role in HDM + DEP induced AHR.…”

Section: Discussionmentioning

confidence: 99%

“…While this manuscript was being finalized, a study by De Grove et al came to a similar conclusion. 22 The authors exposed C57Bl/6 mice intranasally on days 1, 8 and 15 to either saline, DEP (25 μg F I G U R E 6 IL33 signaling in T-cells is contributing to allergen-induced Th2/Th17 responses. A, Experimental protocol.…”

Section: Discussionmentioning

confidence: 99%

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IL33 contributes to diesel pollution‐mediated increase in experimental asthma severity

Brandt

Bolcas

Ruff

et al. 2020

Allergy

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Background Exposure to traffic pollution, notably diesel exhaust particles (DEP), increases risk for asthma and asthma exacerbations. The contribution of cytokines generated by stressed lung epithelial cells (IL25, IL33, TSLP) to DEP‐induced asthma severity remains poorly understood. Methods BALB/c mice were exposed intratracheally once to DEP or 9 times over 3‐weeks to either saline, DEP, and/or house dust mite extract (HDM). Airway hyper‐responsiveness (AHR), pulmonary inflammation, and T‐cell subsets were assessed 24 hours after the last exposure in mice sufficient and deficient for the IL33 receptor ST2. Results DEP exposure induces oxidative stress, IL6, neutrophils and pulmonary accumulation of IL33, but not IL25 or TSLP or other features of allergic disease. When mice are co‐exposed to DEP and low doses of HDM, DEP increases IL33 lung levels and Th2 responses. ST2 deficiency partially protected mice from HDM + DEP induced AHR in association with decreased type 2 inflammation and lung levels of IL5+IL17A+ co‐producing T‐cells. Upon in vitro HDM challenge of lung cells from HDM ± DEP exposed ST2−/− mice, secretion of IL5, IL13, IL6 and IL17A was abrogated by a mechanism involving IL33 signaling in both dendritic cells and T‐cells. HDM + DEP exposed bone marrow derived dendritic cells and IL33 pulsed BMDC promote a mixed Th2/Th17 response that was dependent on ST2 expression by CD4+ T‐cells. Conclusion IL33 contributes to DEP mediated increase in allergen‐induced Th2 inflammation and AHR in a mouse model of severe steroid resistant asthma, potentially through the accumulation of pathogenic IL5+IL17A+ CD4+ effector T‐cells.

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Quantification and role of innate lymphoid cell subsets in Chronic Obstructive Pulmonary Disease

et al. 2021

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Objectives Innate lymphoid cells (ILCs) secrete cytokines, such as IFN‐γ, IL‐13 and IL‐17, which are linked to chronic obstructive pulmonary disease (COPD). Here, we investigated the role of pulmonary ILCs in COPD pathogenesis. Methods Lung ILC subsets in COPD and control subjects were quantified using flow cytometry and associated with clinical parameters. Tissue localisation of ILC and T‐cell subsets was determined by immunohistochemistry. Mice were exposed to air or cigarette smoke (CS) for 1, 4 or 24 weeks to investigate whether pulmonary ILC numbers and activation are altered and whether they contribute to CS‐induced innate inflammatory responses. Results Quantification of lung ILC subsets demonstrated that ILC1 frequency in the total ILC population was elevated in COPD and was associated with smoking and severity of respiratory symptoms (COPD Assessment Test [CAT] score). All three ILC subsets localised near lymphoid aggregates in COPD. In the COPD mouse model, CS exposure in C57BL/6J mice increased ILC numbers at all time points, with relative increases in ILC1 in bronchoalveolar lavage (BAL) fluid. Importantly, CS exposure induced increases in neutrophils, monocytes and dendritic cells that remained elevated in Rag2 / Il2rg ‐deficient mice that lack adaptive immune cells and ILCs. However, CS‐induced CXCL1, IL‐6, TNF‐α and IFN‐γ levels were reduced by ILC deficiency. Conclusion The ILC1 subset is increased in COPD patients and correlates with smoking and severity of respiratory symptoms. ILCs also increase upon CS exposure in C57BL/6J mice. In the absence of adaptive immunity, ILCs contribute to CS‐induced pro‐inflammatory mediator release, but are redundant in CS‐induced innate inflammation.

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IL‐33 signalling contributes to pollutant‐induced allergic airway inflammation

Abstract: Our data suggest that the IL-33/ST2 pathway contributes to the onset of DEP-enhanced allergic airway inflammation.

Cited by 34 publications

References 44 publications

Bifidobacterium breve M‐16V alters the gut microbiota to alleviate OVA‐induced food allergy through IL‐33/ST2 signal pathway

Bifidobacterium breve M‐16V alters the gut microbiota to alleviate OVA‐induced food allergy through IL‐33/ST2 signal pathway

IL33 contributes to diesel pollution‐mediated increase in experimental asthma severity

Quantification and role of innate lymphoid cell subsets in Chronic Obstructive Pulmonary Disease

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