Innate lymphoid cells in asthma

Vercelli, Donata; Gozdz, Justyna; Mutius, Erika von

doi:10.1097/aci.0000000000000023

Cited by 24 publications

(7 citation statements)

References 32 publications

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“…Schuster et al also demonstrated in an airway inflammation model that n-3 PUFAs had a tendency to increase IL-5 secretion [23]. It is important to note that IL-5 is implicated in the pathogenesis of several diseases, particularly lung inflammatory conditions such as asthma [24]. The findings from this study and others imply that an enhancement in IL-5 secretion in humans could have negative consequences for inflammatory lung diseases.…”

Section: Discussionsupporting

confidence: 57%

Short-term consumption of n-3 PUFAs increases murine IL-5 levels, but IL-5 is not the mechanistic link between n-3 fatty acids and changes in B-cell populations

Teague

Harris

Whelan

et al. 2016

The Journal of Nutritional Biochemistry

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N-3 polyunsaturated fatty acids (PUFA) exert immunomodulatory effects on B cells. We previously demonstrated that n-3 PUFAs enhanced the relative percentage and/or frequency of select B2 cell subsets. The objectives here were to determine if n-3 PUFAs: i) could boost cytokines that target B cell frequency, ii) enhance the frequency of the B1 population and iii) to identify the mechanism by which n-3 PUFAs modify the proportion of B cells. Administration of n-3 PUFAs as fish oil to C57BL/6 mice enhanced secretion of the Th2 cytokine IL-5 but not IL-9 or IL-13. N-3 PUFAs had no influence on the percentage or frequency of peritoneal B1 or B2 cells. Subsequent experiments with IL-5−/− knockout mice showed n-3 PUFAs decreased the percentage of bone marrow B220loIgMhi cells and increased the proportion and number of splenic IgM+IgDloCD21lo cells compared to the control. These results, when compared with our previous findings with wild type mice, suggested IL-5 had no role in mediating the effect of n-3 PUFAs on B cell populations. To confirm this conclusion, we assayed IL-5 secretion in a diet-induced obesity model in which n-3 PUFAs enhanced the frequency of select B cell subsets. N-3 PUFA supplementation as ethyl esters to obesogenic diets did not alter circulating IL-5 levels. Altogether, the data establish that n-3 PUFAs as fish oil can increase circulating IL-5 in lean mice, which has implications for several disease endpoints, but this increase in IL-5 is not the mechanistic link between n-3 PUFAs and changes in B cell populations.

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Section: Discussionsupporting

confidence: 57%

Short-term consumption of n-3 PUFAs increases murine IL-5 levels, but IL-5 is not the mechanistic link between n-3 fatty acids and changes in B-cell populations

Teague

Harris

Whelan

et al. 2016

The Journal of Nutritional Biochemistry

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“…TSLP activates dendritic cells 9 and also directly promotes naive CD4 + T cells to into type 2 helper T cells (Th2 cells) 10 . IL-25, IL-33, and TSLP can stimulate group 2 innate lymphoid cells (ILC2) to release type 2 cytokines 11 – 14 . IL-25 15 – 18 , IL-33 19 , and TSLP 10 have each been reported to be both necessary and sufficient for type 2 production, eosinophilic airway inflammation, mucous metaplasia, and airway hyperresponsiveness in mouse asthma models.…”

Section: Introductionmentioning

confidence: 99%

Intelectin contributes to allergen-induced IL-25, IL-33, and TSLP expression and type 2 response in asthma and atopic dermatitis

Cheng

Zhang

et al. 2017

Mucosal Immunology

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The epithelial and epidermal innate cytokines IL-25, IL-33, and thymic stromal lymphopoietin (TSLP) play pivotal roles in the initiation of allergic inflammation in asthma and atopic dermatitis. However, the mechanism by which the expression of these innate cytokines is regulated remains unclear. Intelectin (ITLN) is expressed in airway epithelial cells and promotes allergic airway inflammation. We hypothesized that ITLN is required for allergen-induced IL-25, IL-33 and TSLP expression. In two asthma models, Itln knockdown reduced allergen-induced increases in Il-25, Il-33, and Tslp and development of type 2 response, eosinophilic inflammation, mucus overproduction, and airway hyperresponsiveness. Itln knockdown also inhibited house dust mite (HDM)-induced early upregulation of Il-25, Il-33, and Tslp in a model solely inducing airway sensitization. Using human airway epithelial cells, we demonstrated that HDM-induced increases in ITLN led to phosphorylation of EGFR and ERK which were required for induction of IL-25, IL-33, and TSLP expression. In two atopic dermatitis models, Itln knockdown suppressed expression of Il-33, Tslp and Th2 cytokines and eosinophilic inflammation. In humans, ITLN1 expression was significantly increased in asthmatic airways and in lesional skin of atopic dermatitis. We conclude that intelectin contributes to allergen-induced Il-25, Il-33 and Tslp expression in asthma and atopic dermatitis.Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use

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“…Innate Lymphoid Cells Innate lymphoid cells (ILCs) are non-T, non-B effector cells that show high levels of effector cell functions (mainly cytokine production) upon activation [106]. ILCs are involved in tissue homeostasis, repair, and remodeling, as well as innate immunity [107].…”

Section: Fungal Asthma-associated Inflammationmentioning

confidence: 99%

Allergic Inflammation in Aspergillus fumigatus-Induced Fungal Asthma

Ghosh

Hoselton

Schuh

2015

Curr Allergy Asthma Rep

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Although fungi are pervasive in many environments, few cause disease in humans. Of these, Aspergillus fumigatus is particularly well suited to be a pathogen of the human lung. Its physical and biological characteristics combine to provide an organism that can cause tremendous morbidity and high mortality if left unchecked. Luckily, that is rarely the case. However, repeated exposure to inhaled A. fumigatus spores often results in an immune response that carries significant immunopathology, exacerbating asthma and changing the structure of the lung with chronic impacts to pulmonary function. This review focuses on the current understanding of the mechanisms that are associated with fungal exposure, sensitization, and infection in asthmatics, as well as the function of various inflammatory cells associated with severe asthma with fungal sensitization.

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Innate lymphoid cells in asthma

Abstract: Although the limited success of these trials is often quoted to dismiss the role of Th2 immunity as a whole, we propose that Th2 cytokines released by ILC2s may be critical for human asthma, but are not adequately neutralized because they are not readily accessible in peripheral tissues.

Cited by 24 publications

References 32 publications

Short-term consumption of n-3 PUFAs increases murine IL-5 levels, but IL-5 is not the mechanistic link between n-3 fatty acids and changes in B-cell populations

Short-term consumption of n-3 PUFAs increases murine IL-5 levels, but IL-5 is not the mechanistic link between n-3 fatty acids and changes in B-cell populations

Intelectin contributes to allergen-induced IL-25, IL-33, and TSLP expression and type 2 response in asthma and atopic dermatitis

Allergic Inflammation in Aspergillus fumigatus-Induced Fungal Asthma

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