The Immunomodulatory Effects of Royal Jelly on Defending Against Bacterial Infections in the Caenorhabditis elegans Model.

Emerging evidence suggests that aging is associated with the deterioration of immunity, a term known as immunosenescence, which may lead to a higher incidence of infections in the elderly population. Our previous studies reported that supplementation of royal jelly (RJ) extended the lifespan of Caenorhabditis elegans (C. elegans), a nematode model. The aim of this study was to investigate the potential benefits of RJ supplementation on modulation of the innate immunity in C. elegans. Using Staphylococcus aureus (S. aureus; ATCC 25923) as the infection model, we showed that RJ supplementation from the egg hatching stage could protect C. elegans against the infection. Further mechanistic studies demonstrated that RJ coordinated pathways of IIS/DAF-16, p38 MAPK, and Wnt to modulate the innate immunity. In addition, when RJ was administrated to the aged C. elegans, the worms displayed prolonged survival time to a variety of bacterial infections compared with the nontreatment group. This result indicates the RJ may help delay the innate immunosenescence.

Cranberry extract standardized for proanthocyanidins promotes the immune response of Caenorhabditis elegans to Vibrio cholerae through the p38 MAPK pathway and HSF-1.

Botanicals are rich in bioactive compounds, and some offer numerous beneficial effects to animal and human health when consumed. It is well known that phytochemicals in cranberries have anti-oxidative and antimicrobial activities. Recently, an increasing body of evidence has demonstrated that cranberry phytochemicals may have potential benefits that promote healthy aging. Here, we use Caenorhabditis elegans as a model to show that water-soluble cranberry extract standardized to 4.0% proanthocyanidins (WCESP), a major component of cranberries, can enhance host innate immunity to resist against Vibrio cholerae (V. cholerae; wild type C6706 (O1 El Tor biotype)) infection. Supplementation of WCESP did not significantly alter the intestinal colonization of V. cholerae, but upregulated the expression of C. elegans innate immune genes, such as clec-46, clec-71, fmo-2, pqn-5 and C23G10.1. Additionally, WCESP treatment did not affect the growth of V. cholerae and expression of the major bacterial virulence genes, and only slightly reduced bacterial colonization within C. elegans intestine. These findings indicate that the major components of WCESP, including proanthocyanidins (PACs), may play an important role in enhancing the host innate immunity. Moreover, we engaged C. elegans mutants and identified that the p38 MAPK signaling, insulin/IGF-1 signaling (IIS), and HSF-1 play pivotal roles in the WCESP-mediated host immune response. Considering the level of conservation between the innate immune pathways of C. elegans and humans, the results of this study suggest that WCESP may also play an immunity-promoting role in higher order organisms.