Vitamin D enhances production of soluble ST2, inhibiting the action of IL-33

Pfeffer, Paul; Chen, Yin-Huai; Woszczek, Grzegorz; Matthews, Nick; Chevretton, Elfy B; Gupta, Atul; Saglani, Sejal; Bush, Andrew; Corrigan, Christopher; Cousins, David J.; Hawrylowicz, Catherine M.

doi:10.1016/j.jaci.2014.09.044

Cited by 49 publications

(45 citation statements)

References 10 publications

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“…Further, low levels of vitamin D and hypoparathyroidism are associated with cardiomyopathy remodeling and worsening of HF [78]. Furthermore, calcitriol, the biologically active form of vitamin D, regulates cardiac function and might modulate ST2 [79]. Thus, interrelations of the vitamin D/PTH axis and sST2 regulating inflammation and fibrosis in the heart may also regulate the HF.…”

Section: Cardiac Diseasesmentioning

confidence: 99%

Role of Vitamin D in Cardiovascular Diseases

Rai

Agrawal

2017

Endocrinology and Metabolism Clinics of North America

122

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Vitamin D is critical in mineral homeostasis and skeletal health, and plays regulatory role in non-skeletal tissues. Vitamin D deficiency is associated with chronic inflammatory diseases, including diabetes and obesity both being strong risk factors for cardiovascular diseases (CVD). CVD, including coronary artery disease, myocardial infarction, hypertrophy, cardiomyopathy, cardiac fibrosis, heart failure, aneurysm, peripheral arterial disease, hypertension, and atherosclerosis, are major causes of morbidity and mortality worldwide. The association of these diseases with vitamin D deficiency and improvement with vitamin D supplementation suggest its therapeutic benefit. Here, we critically review the recent findings on the association of vitamin D deficiency and CVD.

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Section: Cardiac Diseasesmentioning

confidence: 99%

Role of Vitamin D in Cardiovascular Diseases

Rai

Agrawal

2017

Endocrinology and Metabolism Clinics of North America

122

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“…It has been demonstrated recently that 25(OH)-VitD3 enhances production of the soluble ST2 isoform [16].…”

Section: Sst2 In Serum Was Reduced By Rv In Vivo In Control and In Asmentioning

confidence: 99%

“…During an allergen and rhinovirus (RV)-induced asthma exacerbation in vivo, IL-33 and IL-25 (IL-17E) [10] are released from the infected necrotic airway epithelial cells, leading to the activation of IL-33-responsive IL-33R/ST2 1 T cells in general, and specifically to the activation of ILC2s [11], which are key effector cells releasing Th2 cytokines such as IL-13 and IL-5, thus linking viral infection and the exacerbation of asthma [12][13][14]. Moreover, it has been demonstrated recently that 25(OH)-VitD3 enhances production of the soluble ST2 isoform [16]. Moreover, it has been demonstrated recently that 25(OH)-VitD3 enhances production of the soluble ST2 isoform [16].…”

Section: Introductionmentioning

confidence: 99%

“…ST2 is encoded by IL-1RL1, and after differential gene splicing it can produce a functional membrane-bound receptor (IL-33R or ST2L) or soluble decoy receptor (sST2), depending on the splice variant [15]. Moreover, it has been demonstrated recently that 25(OH)-VitD3 enhances production of the soluble ST2 isoform [16]. Because soluble sST2 neutralizes the effect of IL-33, sST2 is considered an anti-inflammatory factor in asthma [17,18].…”

Section: Introductionmentioning

confidence: 99%

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Soluble ST2 regulation by rhinovirus and 25(OH)-vitamin D3 in the blood of asthmatic children

Haag

Sharma

Rauh

et al. 2018

Clinical and Experimental Immunology

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Paediatric asthma exacerbations are often caused by rhinovirus (RV). Moreover, 25(OH)-vitamin D3 (VitD3) deficiency during infancy was found associated with asthma. Here, we investigated the innate immune responses to RV and their possible modulation by 25(OH)-VitD3 serum levels in a preschool cohort of children with and without asthma. The innate lymphoid cell type 2 (ILC2)-associated marker, ST2, was found up-regulated in the blood cells of asthmatic children with low serum levels of 25(OH)-VitD3 in the absence of RV in their airways. Furthermore, in blood cells from control and asthmatic children with RV in their airways, soluble (s) ST2 (sST2) protein was found reduced. Asthmatic children with low 25(OH)-VitD3 in serum and with RV in vivo in their airways at the time of the analysis had the lowest sST2 protein levels in the peripheral blood compared to control children without RV and high levels of 25(OH)-VitD3. Amphiregulin (AREG), another ILC2-associated marker, was found induced in the control children with RV in their airways and low serum levels of 25(OH)-VitD3. In conclusion, the anti-inflammatory soluble form of ST2, also known as sST2, in serum correlated directly with interleukin (IL)-33 in the airways of asthmatic children. Furthermore, RV colonization in the airways and low serum levels of 25(OH)-VitD3 were found to be associated with down-regulation of sST2 in serum in paediatric asthma. These data indicate a counter-regulatory role of 25(OH)-VitD3 on RV-induced down-regulation of serum sST2 in paediatric asthma, which is relevant for the therapy of this disease.

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“…In addition to the transmembrane ST2, soluble ST2 (sST2) is produced by the epithelium and functions as a decoy receptor, neutralizing the effects of IL-33 [66]. Consistent with the proposed protective effects of sST2, vitamin D is a potent inducer of sST2 production in bronchial epithelial cells [67], and vitamin D insufficiency is associated with several allergic diseases [68]. Surprisingly, sST2 is elevated in several diseases like asthma and ulcerative colitis and may suggest an attempt to control aberrant IL-33.…”

Section: Introductionmentioning

confidence: 99%

Epithelial Cell Regulation of Allergic Diseases

Gour

Lajoie

2016

Curr Allergy Asthma Rep

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Allergic diseases, which have escalated in prevalence in recent years, arise as a result of maladaptive immune responses to ubiquitous environmental stimuli. Why only certain individuals mount inappropriate type 2 immune responses to these otherwise harmless allergens has remained an unanswered question. Mounting evidence suggests that the epithelium, by sensing its environment, is the central regulator of allergic diseases. Once considered to be a passive barrier to allergens, epithelial cells at mucosal surfaces are now considered to be the cornerstone of the allergic diathesis. Beyond their function as maintaining barrier at mucosal surfaces, mucosal epithelial cells through the secretion of mediators like IL-25, IL-33, and TSLP control the fate of downstream allergic immune responses. In this review, we will discuss the advances in recent years regarding the process of allergen recognition and secretion of soluble mediators by epithelial cells that shape the development of the allergic response.

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Vitamin D enhances production of soluble ST2, inhibiting the action of IL-33

Cited by 49 publications

References 10 publications

Role of Vitamin D in Cardiovascular Diseases

Role of Vitamin D in Cardiovascular Diseases

Soluble ST2 regulation by rhinovirus and 25(OH)-vitamin D3 in the blood of asthmatic children

Epithelial Cell Regulation of Allergic Diseases

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