Aging is accompanied by remodeling of the immune system. With time, this leads to a decline in immune efficacy, resulting in increased vulnerability to infectious diseases, diminished responses to vaccination, and a susceptibility to age-related inflammatory diseases. An age-associated immune alteration, extensively reported in previous studies, is the reduction in the number of peripheral blood naïve cells, with a relative increase in the frequency of memory cells. These two alterations, together with inflamm-aging, are considered the hallmarks of immunosenescence. Because aging is a plastic process, it is influenced by both nutritional and pharmacological interventions. Therefore, the role of nutrition and of immunomodulation in immunosenescence is discussed, due to the multifactorial influence on these hallmarks. The close connection between nutrition, intake of bioactive nutrients and supplements, immune function, and inflammation demonstrate the key role of dietary strategies as regulators of immune response and inflammatory status, hence as possible modulators of the rate of immunosenescence. In addition, potential options for therapeutic intervention are clarified. In particular, the use of interleukin-7 as growth factor for naïve T cells, the function of checkpoint inhibitors in improving T cell responses during aging and, the potential of drugs that inhibit mitogen-activated protein kinases and their interaction with nutrient signaling pathways are discussed. Finally, it is suggested that the inclusion of appropriate combinations of toll-like receptor agonists may enhance the efficacy of vaccination in older adults.

Astaxanthin, a xanthophyll carotenoid, is a secondary metabolite naturally synthesized by a number of bacteria, microalgae, and yeasts. The commercial production of this pigment has traditionally been performed by chemical synthesis, but the microalga Haematococcus pluvialis appears to be the most promising source for its industrial biological production. Due to its collective diverse functions in skin biology, there is mounting evidence that astaxanthin possesses various health benefits and important nutraceutical applications in the field of dermatology. Although still debated, a range of potential mechanisms through which astaxanthin might exert its benefits on skin homeostasis have been proposed, including photoprotective, antioxidant, and anti-inflammatory effects. This review summarizes the available data on the functional role of astaxanthin in skin physiology, outlines potential mechanisms involved in the response to astaxanthin, and highlights the potential clinical implications associated with its consumption.

Cocoa and its products are rich sources of polyphenols such as flavanols. These compounds exert antioxidant and anti-inflammatory activities, accountable for cocoa health-promoting effects. However, cocoa polyphenols are poorly absorbed in the intestine, and most of them cannot reach the systemic circulation in their natural forms. Instead, their secondary bioactive metabolites are bioavailable, enter the circulation, reach the target organs, and exhibit their activities. In fact, once reaching the intestine, cocoa polyphenols interact bidirectionally with the gut microbiota. These compounds can modulate the composition of the gut microbiota exerting prebiotic mechanisms. They enhance the growth of beneficial gut bacteria, such as Lactobacillus and Bifidobacterium, while reducing the number of pathogenic ones, such as Clostridium perfringens. On the other hand, bioactive cocoa metabolites can enhance gut health, displaying anti-inflammatory activities, positively affecting immunity, and reducing the risk of various diseases. This review aims to summarize the available knowledge of the bidirectional interaction between cocoa polyphenols and gut microbiota with their various health outcomes.

Objective: Berries are a rich source of anthocyanins, and clinical data suggest that a polyphenol-rich diet may exert health-promoting effects by reducing oxidative stress. The aim of this study was to elucidate the effects of dietary supplementation with Delphinol (trademark owned by MNL Chile) standardized maqui berry (Aristotelia chilensis) extract on products of lipid peroxidation in healthy, overweight, and smoker subjects. Methods: In a double-blind, placebo-controlled design, 42 participants (age 45–65 years) consumed in random order either a standardized extract of maqui berry (162 mg anthocyanins) or a matched placebo, given 3 times daily for 4 weeks. The samples were collected at baseline, after the end of the supplementation, and 40 days after the end of the study. Primary outcome was the measure of oxidized low-density lipoprotein (Ox-LDL) and F₂-isoprostanes in plasma and urine, respectively. Secondary outcomes included anthropometric measures, blood pressure, and lipid profile. Results: Delphinol supplementation was associated with reduced levels of Ox-LDL in the anthocyanin group compared to baseline (p < 0.05). There was also a decrease in urinary F₂-isoprostanes (8-iso-prostaglandin F2α) at 4 weeks versus baseline in the Delphinol-supplemented group (p < 0.05). However, no differences in primary outcomes were evident at 40 days of follow-up. In the fourth week of the intervention, no significant differences were noted for anthropometric characteristics, ambulatory blood pressure, and lipid profile. Conclusions: Our observations suggest that dietary interventions with maqui berry extract may improve oxidative status (Ox-LDL and F₂-isoprostanes) in healthy adults, overweight adults, and adult smokers.

Astaxanthin (AST) is a dietary xanthophyll predominantly found in marine organisms and seafood. Due to its unique molecular features, AST has an excellent antioxidant activity with a wide range of applications in the nutraceutical and pharmaceutical industries. In the past decade, mounting evidence has suggested a protective role for AST against a wide range of diseases where oxidative stress and inflammation participate in a self-perpetuating cycle. Here, we review the underlying molecular mechanisms by which AST regulates two relevant redox-sensitive transcription factors, such as nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor κB (NF-κB). Nrf2 is a cellular sensor of electrophilic stress that coordinates the expression of a battery of defensive genes encoding antioxidant proteins and detoxifying enzymes. Likewise, NF-κB acts as a mediator of cellular stress and induces the expression of various pro-inflammatory genes, including those encoding cytokines, chemokines, and adhesion molecules. The effects of AST on the crosstalk between these transcription factors have also been discussed. Besides this, we summarize the current clinical studies elucidating how AST may alleviate the etiopathogenesis of oxidative stress and inflammation.