Vitamin D deficiency is associated with

Vitamin D deficiency is associated with food sensitization (Baek et al., 2014), as well as IgE-mediated food allergy (Allen et al., 2013). Infants from Australian-born parents with vitamin D insufficiency had increased likelihood of egg and peanut allergy (Allen et al., 2013). By contrast, elevated levels of vitamin D during pregnancy and at birth have been associated with high risk of food allergy (Weisse et al., 2013). The frequency of food allergy/anaphylaxis is higher at higher absolute latitudes where there is insufficient UVB intensity in the autumn and winter months for adequate vitamin D synthesis (Mullins and Camargo, 2012). Low vitamin D results in compromised barrier function, altered microbial composition of the gut, and together with effects on antigen presenting cells and T cells predisposes an individual to allergic responses to food Glycerol (Vassallo and Camargo, 2010). Other dietary factors that suppress food allergy include aryl hydrocarbon receptor ligands, found in cruciferous vegetables such as cabbage, Brussels sprouts, and broccoli (Schulz et al., 2011). Ingestion of n−3 long chain polyunsaturated fatty acids (PUFA), and non-digestible oligosaccharides can also suppress food allergy in mice through induction of Tregs (Schouten et al., 2012; Van Den Elsen et al., 2013). Dietary factors may be directly immunomodulatory, or may suppress food allergy through modulation of the intestinal microbiota (Wu et al., 2011). See Fig. 2 for a schematic illustrating the role of microbiota and the diet in allergy and tolerance to foods.
Emerging treatments for food allergy
Search strategy and selection criteria Data for this review were identified by searches in PubMed. The references were selected based on the most impactful journals and, when possible, published in the last 5years. Only articles published in English were included.
Conflict of interest
Introduction As aging populations grow, sight loss is becoming a major world health concern. Eye conditions related to aging share some common pathological characteristics, including the degeneration of the retinal pigment epithelium (RPE) (Ambati et al., 2003) and secondary photoreceptor cell damage (Organisciak and Vaughan, 2010). Several lines of evidence have determined oxidative stress in the RPE to be a major pathogenic element in age-related macular degeneration (AMD) (Shen et al., 2007) and diabetic retinopathy (Du et al., 2013). Oxidative stress refers to elevated intracellular levels of reactive oxygen species (ROS) (Cross et al., 1987), which are produced by damaged mitochondria and which inevitably impair cellular function (Balaban et al., 2005). Recently, oxidative stress was shown to induce an age-dependent increase in ROS levels and cell death in human RPE (He et al., 2014). However, the molecular mechanisms making aging RPE vulnerable to high levels of ROS and subsequent activation of cell death are largely unknown. We have recently identified the neuroprotective role of prolactin (PRL) in rat retinas (Arnold et al., 2014). PRL is a critical link between the neuroendocrine and immune systems. Notably, deep sequencing experiments showed that increased vulnerability to AMD is due to initially high levels of inflammatory factors and low levels of homeostatic neuroprotective factors, such as the suppressor of cytokine signaling (SOCS) 1 (Mustafi et al., 2012; Swaroop et al., 2009). PRL signaling is down-regulated when SOCS-1 is lost (Minoo et al., 2004). Together, these findings indicate that PRL signaling may play a critical role in the age-related degeneration of the retina. PRL and its receptor are expressed in the retina (Rivera et al., 2008). Retinas from PRL receptor knockout (prlr−/−) mice exhibit photoresponsive dysfunction that correlates with reduced rhodopsin levels (Arnold et al., 2014). Given that the RPE normally supplies photopigments to rods (Nandrot et al., 2008), a lack of PRL signaling may alter its function. A previous study demonstrated that most retinal cells are positive for the PRL receptor (Rivera et al., 2008), but whether this receptor is present in the RPE remains to be determined.