Vasoactive intestinal peptide(SkyePharma Plc)

The role of neuro-immune interaction in allergic diseases, a group of common immune system diseases, has garnered increasing attention. Neuropeptides, as a crucial component of neuro-immune crosstalk with local neuroendocrine and signaling functions, play a significant role that must not be overlooked. Neuropeptides are released by neurons and even some immune cells, and mediate neuro-immune crosstalk by activating relevant specific receptors on immune cells. Recent studies have found that neuropeptides have a certain regulatory effect on allergic diseases, which could be beneficial or detrimental for the development of allergic diseases. Nevertheless, the precise mechanism of neuropeptides in allergic diseases remains unclear, particularly in the context of food allergy where their role is poorly understood. This review summarized the interplay between neuropeptides and different immune cells, as well as their current research progress in several common allergic diseases: atopic dermatitis, allergic asthma, and food allergy. It is evident that neuropeptides such as substance P, calcitonin gene-related peptide, vasoactive intestinal peptide, and neuromedin U, exert important regulatory effects on allergic diseases, yet further investigation is required to fully elucidate their mechanisms of action, which may contribute to better understanding of the onset and progression of allergic diseases and finding better immunomodulatory strategies.

Several neuropeptides present in bone tissues, produced by nerve fibers and bone cells, have been reported to play a role in regulating the fine‐tuning of osteoblast and osteoclast functions to maintain bone homeostasis. This study aims to characterize the influence of the neuropeptide vasoactive intestinal peptide (VIP) on the differentiation process of human mesenchymal stem cells (MSCs) into osteoblasts and on their anabolic function. We describe the mRNA and protein expression profile of VIP and its receptors in MSCs as they differentiate into osteoblasts, suggesting the presence of an autocrine signaling pathway in these cells. Our findings reveal that VIP enhances the expression of early osteoblast markers in MSCs under osteogenic differentiation and favors both bone matrix formation and proper cytoskeletal reorganization. Finally, our data suggest that VIP could be exerting a direct modulatory role on the osteoblast to osteoclast signaling by downregulating the receptor activator of nuclear factor‐κB ligand/osteoprotegerin ratio. These results highlight the potential of VIP as an osteoinductive differentiation factor, emerging as a key molecule in the maintenance of human bone homeostasis.