Program Agenda

1. Most studies of mechanisms look at one specific nutrient. Is there any evidence of synergy (or antagonism) between different micronutrients in terms of immunomodulation?
2. What is the influence of disease on the absorption of micronutrients and on micronutrient status?
3. A reduction of plasma retinol, zinc and iron are a consequence of Infection. Why does this happen? Low plasma iron stimulates greater activity of macrophage nitric oxide synthase activity which is bacteriocidal. Is the reduction in retinol a device to reduce losses of urinary retinol which are associated with fever? Alternatively, does low retinol increase immunocompetance?
4. How does Vitamin A (or other micronutrients) affect the number and differentiation of bone marrow progenitors? Are significant effects seen with a moderate deficiency of the particular micronutrient in question?
5. What is the interaction of vitamin A and acute phase response to infection/injury? When is this interaction "beneficial" to the host and when does it represent maladaptation? 

1. How can researchers make the best use of the many emerging transgenic and gene-deletion (knock-out) mice? 
2. What animal models are particularly suited for evaluating the immunomodulatory effects of nutrients on the maturation, activation and effector functions of the various immune cells types and tissues? Which biomarkes, in vivo tests, provide the best insights when considering the modulatory influences of nutrients on immunocompetence.
3. What molecular studies can be done to address micronutrient modulation of immune function during infection in humans? How do we bridge the large gap between molecular biology and nutritional epidemiology?
4. When, where and how do the pathways of retinoic acid and cytokine signaling intersect? Do Th1 type cytokines markedly enhance Th2 responses in vitamin A (or other micronutrient) deficiency? Are there key intermediates, such as IRF, STAT or JAK/TYK signaling pathways?
5. Why is plasma zinc moved to the liver in infection? Is it just to reduce losses via the gut in diarrhoea or does low plasma Zn upregulate aspects of the immune system?

1. Since compartmentalization is an important component of the way the immune response is regulated in vivo, how does the reliance on tissue immune cells (e.g., peritoneal macrophages, splenocytes) in most rodent studies versus peripheral blood immune cells for human studies effect the comparability of these data?
2. Are cell lines particularly useful in assessing the impact of nutrient status on specific aspects (B cells, Macrophages or interactions among) of innate vs acquired immunity?
3. How should one select the most appropriate cell or animal model that would relate these studies to humans?
4. Does vitamin A deficiency represent a condition of chronic (mild) inflammation that biases the immune system towards Th1 type of response?

1. What are the practical issues pertaining to the inclusion of state-of-the-art immunological parameters in field studies?
2. What are the public health implications of nutritional immunology? Can we design specific micronutrient interventions for specific infectious diseases? Is it time to form a professional society of nutritional immunology? What has had more of an impact on infectious disease case fatality rates in developing countries--better nutrition or technologically advanced medicine?
3. What are the consequences of marginal vs frank deficiencies and are there markers of marginal deficiencies applicable to field situations? Are micronutrient effects linked to macronutrient status?
4. Considering the importance of the ultimate move from "bench to bedside", in the field of nutrition and infectious diseases, what factors/issues should be considered in establishing guidelines/standards. For example, is a Board of nutrition and ID experts needed?