Can Nutrition Help Prevent Common Cold & Flu Viruses? - Center for Nutrition Studies
Notably, infection with influenza A virus induced A robust, dose-response association was found between lower. In contrast, Pozzetto and colleagues (7) reported no relationship of protein status to postvaccinal antibody response to influenza viruses in older humans. In addition, the relationship between adequate nutrition and immune function has been repeatedly demonstrated. Mouse models provide strong evidence that.
In this review, we will describe evidence for the role of vitamin D in modulating the adaptive and innate immune response.
We will then consider how those aspects of the immune system respond to influenza infection. We will also consider observational studies and randomized controlled trials of vitamin D supplementation in humans and the concurrent seasonality of poor vitamin D status and increased risk of influenza infection.
Finally, we will note the problems in accurately assessing vitamin D and consider the next steps for assessing vitamin D in the context of respiratory illness. Current status of knowledge Vitamin D and adaptive immune response to infection The adaptive immune response to infection is complex and multi-faceted and involves a diverse population of cell types and other factors such as cytokines, chemokines, enzymes, and hormones 33031 Fig.
Additionally, the immune response to an infectious insult is not static; characteristics of the response measured by serum cytokines in human adults change from the initial period of antigenic stimulation to the later stage of disease clearance Vitamin D may therefore affect one component of an immune system response but not other components, meaning that the net effect of vitamin D on immune function and clinical illness is difficult to characterize.
This also suggests that evidence of vitamin D's role in the immune system in vitro may not apply to vitamin D's role in vivo. Nevertheless, vitamin D [in particular, 1,25 OH 2D] has been found to act on specific cell parameters of the adaptive immune response, most notably T- and B-cells Fig. Figure 1 View large Download slide Vitamin D and its various actions in the immune system. C Vitamin D inhibits the production of B-cells, the differentiation of B-cells into plasma cells, and the production of antibodies by B-cells.
Th, T helper cell; Treg, T regulatory cell. The T-cell profile shift Vitamin D [espcially 1,25 OH 2D] is widely acknowledged to shift the T-cell response profile from a T helper cell Th 1- to a Th2-mediated response by inhibiting cells of the Th1 profile 33133 - 43 in vitro in mouse fibroblasts, pancreatic islets, cultured splenocytes, and host serum; and in vivo in mouse dendritic cells.
Vitamin D also promotes cells of the Th2 profile 313941424445 in mouse fibroblasts Fig.
The Influence of Nutrition on Influenza Virus Infection - Melinda Beck
Complicated interactions between various vitamins and minerals and specific deficiencies related to chronic disease states may account for study-to-study differences in results. Moreover, the benefit of supplementation may only be observed when a nutritional deficiency is reversed.
Thus, study populations may need to be characterized according to underlying chronic disease, the extent of disability, and the associated nutritional deficiencies for that subset of older people. Smaller studies for hypothesis generation and collection of pilot data may be feasible in these well-defined groups of older people. Studies that do not include careful measurement of health indicators including nutritional status may require very large study groups in excess of to adequately power studies, particularly in the institutional setting 9 The most commonly used assay for measuring antibody titers to influenza is the hemagglutination inhibition assay.
Analyzing for differences in seroconversion rates or mean fold increase in antibody titers following vaccination may not be a valid comparison in repeatedly vaccinated older people.
Even though the absolute postvaccination titer is protective, vaccination from the previous year may increase prevaccination titers and diminish the fold increase in antibody titer. The fact that older adults who are vaccinated on an annual basis receive better protection from the vaccine compared to first-time vaccinees suggests that the absolute postvaccination titer is a better surrogate of protection than the mean fold increase.
Seroconversion four-fold rise in antibody titer or seroprotection postvaccination titer greater than or equal to 40 should be considered equivalent measures of the response rates to vaccination.
This type of analysis may have yielded different results in the article by Wouters-Wesseling and colleagues and may account for some of the inconsistent results reported in the literature. Antibody titers measure only the humoral component of the immune response to influenza and do not measure the cellular immune response, which may be more important in older people.
Assays of T-cell responses to influenza stimulation are more labor intensive and need to be applied to smaller groups of well-characterized subjects, including specific nutritional indices to limit the variability of the immunologic responses within study groups.