Vitamin A and D in allergy: from experimental animal models and cellular studies to human disease

Hufnagl, Karin; Jensen‐Jarolim, Erika

doi:10.1007/s40629-018-0054-2

Cited by 44 publications

(32 citation statements)

References 60 publications

(75 reference statements)

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“…Retinoic acid (RA), a biologically active form of vitamin A, has been shown to promote the development and/or elevate the strength of a variety of epithelial and endothelial barriers [17][18][19][20]. While RA has been shown to be effective in reducing inflammation in the airway, these studies have mostly focused on it modulating immune cell differentiation/activity rather than on epithelial cells and barrier function per se [21][22][23]. This study sought to test whether this micronutrient could be useful in elevating basal barrier strength of this bronchial cell culture model as well as determine whether RA can alleviate 16HBE barrier leak triggered by proinflammatory cytokines such as TNF-α and Interleukin-6 (IL-6).…”

Section: Introductionmentioning

confidence: 99%

Retinoic acid improves baseline barrier function and attenuates TNF-α-induced barrier leak in human bronchial epithelial cell culture model, 16HBE 14o-

et al. 2020

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Retinoic acid (RA) has been shown to improve epithelial and endothelial barrier function and development and even suppress damage inflicted by inflammation on these barriers through regulating immune cell activity. This paper thus sought to determine whether RA could improve baseline barrier function and attenuate TNF-α-induced barrier leak in the human bronchial epithelial cell culture model, 16HBE14o- (16HBE). We show for the first time that RA increases baseline barrier function of these cell layers indicated by an 89% increase in transepithelial electrical resistance (TER) and 22% decrease in 14C-mannitol flux. A simultaneous, RA-induced 70% increase in claudin-4 attests to RA affecting the tight junctional (TJ) complex itself. RA was also effective in alleviating TNF-α-induced 16HBE barrier leak, attenuating 60% of the TNF-α-induced leak to 14C-mannitol and 80% of the leak to 14C-inulin. Interleukin-6-induced barrier leak was also reduced by RA. Treatment of 16HBE cell layers with TNF-α resulted in dramatic decrease in immunostaining for occludin and claudin-4, as well as a downward “band-shift” in occludin Western immunoblots. The presence of RA partially reversed TNF-α’s effects on these select TJ proteins. Lastly, RA completely abrogated the TNF-α-induced increase in ERK-1,2 phosphorylation without significantly decreasing the TNF-driven increase in total ERK-1,2. This study suggests RA could be effective as a prophylactic agent in minimizing airway barrier leak and as a therapeutic in preventing leak triggered by inflammatory cascades. Given the growing literature suggesting a “cytokine storm” may be related to COVID-19 morbidity, RA may be a useful adjuvant for use with anti-viral therapies.

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Section: Introductionmentioning

confidence: 99%

Retinoic acid improves baseline barrier function and attenuates TNF-α-induced barrier leak in human bronchial epithelial cell culture model, 16HBE 14o-

et al. 2020

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“…Possible markers for pain syndromes, dysmenorrhea, low back pain and menstrual headache are tissue or even plasma Ca/Mg and vitamin D reduced levels often found in these conditions. The intradermal application of sex hormones in optimal tissue Ca/Mg and vit D microenvironment and optimally standardized technique that induces effective Dendritic/Ts cells inhibiting inflammatory response become an attractive therapeutic method for different clinical situations 13 …”

Section: Discussionmentioning

confidence: 99%

Safety and value of skin test to sex hormones and sex hormone sensitivity desensitization in women with premenstrual syndrome

Itsekson

Yonit²,

Matitiyahu

et al. 2019

World Allergy Organization Journal

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Background Hypersensitivity to one's own sex hormones is not a new concept but it is an underappreciated one. Such a phenomenon may explain a large proportion of symptoms related to the menstrual cycle (such as premenstrual syndrome, PMS), cyclic pain syndromes or unexplained infertility. In this study we propose a novel diagnostic tool of hormonal skin testing which reveals sex hormones sensitivity with high clinical correlation, and a subsequent successful desensitization technique. Methods A group of 35 women with confirmed diagnosis of PMS were enrolled in the study in which they underwent a hormonal skin diagnostic skin testing procedure by intradermal injections of Progesterone (P), Estradiol (E2), Estrone (E1) and Estriol (E3). Skin reaction was monitored, and according to the reaction the patients were treated by serial desensitization by similar serial injections or placebo solvent. Response to treatment was monitored by assessing the change in the severity of PMS related symptoms. Results We show a positive correlation between PMS severity and skin sensitivity to sex hormones. Subsequent desensitization procedure led to a significant improvement in the severity of PMS related symptoms. Conclusions The testing and desensitization procedure is safe, sensitive and bares a high therapeutic potential in approach to resistant hormonal cycle related syndromes. ClinicalTrials.gov Identifier NCT00873262 : Evaluation of Safety/Efficacy of Diagnostic Skin Test Panel and Desensitization Hormone Kit for Treatment of Premenstrual Syndrome (PMS) 2009.

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“…However, recently VitD has gained attention in terms of its possible role in allergic diseases as well. VitD activating enzymes were found, for example, in epithelial cells, T cells, dendritic cells (DC), and activated macrophages [10,11]. According to multiple studies, a substantial portion of the world population has low serum VitD levels.…”

Section: Introductionmentioning

confidence: 99%

“…Activation of VitD occurs in 2 steps: first in the liver, it is modified to a prohormone, followed by conversion to the biological active hormone in the kidneys [16]. As mentioned above, VitD activation also occurs in structural cells and cells of the immune system [10,11]. After VitD is enzymatically activated, it will bind to the nuclear vitamin D receptor (VDR); the VDR will form a homodimer or a heterodimer with retinoic x receptor bound to retinoic acid to activate specific genes in the nucleus.…”

Section: Introductionmentioning

confidence: 99%

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Dietary Vitamin D Supplementation Is Ineffective in Preventing Murine Cow’s Milk Allergy, Irrespective of the Presence of Nondigestible Oligosaccharides

Kerperien

Veening-Griffioen

Oja

et al. 2020

Int Arch Allergy Immunol

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Introduction: Cow’s milk allergy (CMA) is one of the most common food allergies especially early in life. A mixture of nondigestible short-chain galacto-oligosaccharides, long-chain fructo-oligosaccharides, and pectin-derived acidic-oligosaccharides (GFA) may reduce allergy development and allergic symptoms in murine CMA. Recently, vitamin D (VitD) has been suggested to have beneficial effects in reducing allergy as well. Objective: In this study, the immune modulatory effect on allergy prevention using the combination of GFA and VitD was investigated. Methods: Female C3H/HeOuJ mice were fed a control or GFA-containing diet with depleted, standard (1,000 IU/kg), or supplemented (5,000 IU/kg) VitD content for 2 weeks before and during whey sensitization (n = 10–15). Mice were sensitized 5 times intragastrically with PBS as a control, whey as cow’s milk allergen, and/or cholera toxin as adjuvant on a weekly interval. One week after the last sensitization, mice were intradermally challenged in both ear pinnae and orally with whey, subsequently the acute allergic skin response and shock symptoms were measured. After 18 h, terminal blood samples, mesenteric lymph nodes, and spleens were collected. Whey-specific immunoglobulin (Ig) E and IgG1 levels were measured by means of ELISA. T cell subsets and dendritic cells (DCs) were studied using flow cytometry. Results: Additional VitD supplementation did not lower the allergic symptoms compared to the standard VitD diet. CMA mice fed the GFA diet supplemented with VitD (GFA VitD+) significantly decreased the acute allergic skin response of whey sensitized mice when compared to the CMA mice fed VitD (VitD+) group (p < 0.05). The effect of GFA was not improved by extra VitD supplementation even though the CMA mice fed the GFA VitD+ diet had a significantly increased percentage of CD103+ DCs compared to the VitD+ group (p < 0.05). The VitD-deprived mice showed a high percentage of severe shock and many reached the humane endpoint; therefore, these groups were not further analyzed. Conclusions: High-dose VitD supplementation in mice does not protect against CMA development in the presence or absence of GFA.

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Vitamin A and D in allergy: from experimental animal models and cellular studies to human disease

Cited by 44 publications

References 60 publications

Retinoic acid improves baseline barrier function and attenuates TNF-α-induced barrier leak in human bronchial epithelial cell culture model, 16HBE 14o-

Retinoic acid improves baseline barrier function and attenuates TNF-α-induced barrier leak in human bronchial epithelial cell culture model, 16HBE 14o-

Safety and value of skin test to sex hormones and sex hormone sensitivity desensitization in women with premenstrual syndrome

Dietary Vitamin D Supplementation Is Ineffective in Preventing Murine Cow’s Milk Allergy, Irrespective of the Presence of Nondigestible Oligosaccharides

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