Hinweis für Ärzte und Ärztinnen, die mit der Funktion von Vitamin D im Immunsystem, insbesondere bei Erkrankungen der Atemwege, wie Influenza oder Covid19 nicht vertraut sind

In Ergänzung zum Video Dr. Raimund von Helden zum Mechanismus der Infektionsbekämpfung bei Atemwegserkrankungen durch Vitamin D über Defensin und Cathelicidin.

https://www.vitamindservice.de/corona sowie

ttps://www.vitamindservice.de/Coronavirus-live wurden zur Vertiefung nachfolgend Auszüge aus der wissenschaftlichen Publikation:

Int. J. Mol. Sci. 2018, 19, 2419;

https://pubmed.ncbi.nlm.nih.gov/30115864/

zusammengestellt durch Udo Jeske, Bad Liebenwerda, udo@wir-in-bali.de

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„As shown by Beard et al. [4], cathelicidin expression in macrophages and keratinocytes

is induced by CYP27B1, and if there is no 25(OH)D, VDR, or CYP27B1, the ability of these cells to produce cathelicidins is significantly impaired.“

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There are a few arguments which support vitamin D as a likely candidate for the abovementioned “seasonal stimulus”. In summary, most important is the 1α,25(OH) 2 D-stimulated production of AMPs, such as defensin and cathelicidin. As mentioned, these endogenous antibiotics act directly, destroying not only microbial pathogens, but also viruses, including the influenza virus [24,48,49]. The production of cathelicidin is dose-dependent on the serum level of 1α,25(OH) 2 D. As shown by Lang and Samaras [49], 30 ng/mL is necessary for the optimal induction of cathelicidin mRNA, but a higher level of 40 ng/mL was not more efficient. The next argument which supports the antiviral activity of vitamin D is the modulation of the inflammatory response as mentioned above. The release of proinflammatory cytokines by the influenza virus appeared to correlate with the severity of illness [24]. Khare et al. [50] noted that treatment of human lung A549 epithelial cells with 100 or 30 nM of 1α,25(OH) 2 D prior to or post-H1N1 (influenza A virus) exposure significantly decreased the levels of infection-induced TNFα, IFNβ, and IFN-stimulated gene-15 (ISG15) and downregulated IL-8 and IL-6 RNA levels. Following Helming et al. [51], 1α,25(OH) 2 D also potentially diminishes the proinflammatory cytokine production by the modulation of macrophages, which prevents them from the secretion of too many cyto- and chemokines. On the basis of the obtained data, the authors suggested that 1α,25(OH) 2 D participates in a negative feedback loop in which IFNγ-activated macrophages induce the release of 1α,25(OH) 2 D. When this metabolite is accumulated at an efficient concentration, VDR expression is synergistically induced and it translocates into the nucleus. Then, it can suppress the genes making the proinflammatory proteins, such as CCL5, CXCL16, IFI203, FCGR1, FCGR3, TLR2, IRF2, CXCL10, and CXCL9. Tight control of IFNγ responses is crucial for the consequences of granulomatous diseases such as tuberculosis and sarcoidosis [51].

Dieser obige Warnhinweis zu Sarkoidose und Tuberkulose verdient unbedingt Beachtung. Zu Sarkoidose siehe auch:
https://www.vitamindservice.de/faq/was-ist-die-ursache-der-sarkoidose

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Seasonality of Vitamin D Levels and Influenza Rate

Kroll et al. [73] mentioned the other factor conjugated with the level of 25(OH)D and parathyroid hormone (PTH) concentrations, which are known to have a reciprocal seasonal relationship with 25(OH)D. These two compounds vary in sinusoidal pattern throughout the year, even in ergocalciferol-treated patients. This means that 25(OH)D is higher in the summer and lower in winter, while PTH shows the reverse pattern. According to the authors, in these observations, held across three latitudinal regions, both genders and multiple years are applicable for patient care.

Und schließlich zur Rolle von Vitamin D bei Impfungen gegen Rachenwegsinfektionen in der gleichen Publikation mit Stand bereits 2018:

5. Does Vitamin D Affect the Immunogenicity of Influenza Vaccines?

5.1. Vitamin D as an Adjuvant

As shown in this paper, vitamin D undoubtedly plays the role of an immunomodulating agent. Its significance in innate and adaptive immunity prompted scientists to check if there is any influence of vitamin D on the response of the patients to immunization by vaccination with live or inactive attenuated influenza virus, especially because some studies on influenza prevention provide a negative correlation between enhanced post-vaccine immunization and obese patients, whereas obesity implies vitamin D deficits [75,76]. These observations indirectly point to the possible role of vitamin D improvement of the immune response to influenza vaccines. Principi et al. [77] mentioned animal studies in which the results encourage regarding vitamin D as a kind of adjuvant agent for better influenza vaccine efficacy. The studies showed that the addition of vitamin D or 1α,25(OH) 2 D to a variety of vaccine preparations could increase induced immunity to the herpessimplex virus, diphtheria toxoid, tetanus toxoid, hepatitis B surface antigen, poliovirus, or HIVgp160.

5.2.3. Critical Views

The work described and done by Surman et al. [83] raised the very important question of the interaction of different factors resulting in the immune response. The authors reported in mice immunized with an attenuated influenza virus vaccine that double deficiencies for vitamin A and D reduced antibody response in the respiratory tract to a greater extent than deficiency for one of these vitamins. Although supplementation with vitamin A had a greater corrective effect than vitamin D for the restitution of seroprotection (IgG and IgA responses), the best results were with the two vitamins combined and administered at the time of the vaccination of the animals. These studies, although they are animal-based, give some useful information for designing human clinical trials for the improvement of influenza vaccine efficacy and show that the approach to the significance and the potential role of supplementation with micronutrients, such as vitamins, to reach this aim should regard their interaction and synergism of action [74,83].