Industrial By‐Products As a Novel Circular Source of Biocompatible Extracellular Vesicles

Abstract

Extracellular vesicles (EVs) constitute an intricate system of molecular exchange that has recently gained tremendous interest. However, sustainable sources of safe biological EVs remain scarce and elusive. This study explores and defines the use of food industry by-products (BP) as a circular source of safe biocompatible EVs. Averaged diameter and molecular compositions indicate a large yield of exosomes and high abundancy of membrane lipids with signaling capacity in these vesicles. Complex proteomes mimicking those circulating in human blood plasma are also identified. Furthermore, BP-EVs do not show relevant cytotoxicity and display excellent oral and intravenous bioavailability together with specific organ targeting capacity. Collectively, it is believed that the novel findings reported here will open substantial venues for the use of BP as an optimal source of biocompatible nanovesicles in manifold applications of the biotechnological and biomedical fields.

Altered ureido protein modification profiles in seminal plasma extracellular vesicles of non-normozoospermic men

“…Preparations of sEVs were analyzed by nanoparticle tracking analysis (NTA), as we previously indicated ( 8 ). The NTA experiments were performed in triplicate.…”

“…sEVs, also known as prostasomes, are tiny bi-layered vesicles that commonly range in diameter from 30 nm to 1 μm, with exosomes (<250 nm) and microvesicles (>250 nm) being the main components of the distribution ( 6 , 7 ). The membrane of these vesicles is structurally formed by lipids and multidomain proteins, both of which possess outstanding signaling abilities ( 8 ). Furthermore, EVs and prostasomes are known to contain proteins, lipids, and genetic material as cargo, ready to be taken up by the target recipient ( 9 ).…”

Oral Microbiota, Its Equilibrium and Implications in the Pathophysiology of Human Diseases: A Systematic Review

“…Numerous epidemiological studies have implicated oral dysbiosis and infection, specifically periodontal disease, as a significant risk factor associated with CVD [ 78 , 79 , 80 ]; the prevalence of CVD in patients diagnosed with periodontitis is 25–50% higher than in healthy individuals, although the mechanisms of this significant association are unclear [ 70 ]. Periodontal disease caused by dysbiosis and extended oral infection places a vast population of harmful bacterial strains and their secretions, which might involve the presence of extracellular vesicles [ 81 ], in direct contact with disrupted capillary terminals, which in turn introduces these harmful agents into the circulatory system facilitating a global systemic diffusion [ 60 , 79 , 82 ]. Thus, this systemic exposure to oral bacteria and their products probably exerts a significant impact on the onset and progression of CVD through activation of pro-inflammatory processes [ 42 , 83 ].…”

Modifiable Innate Biology within the Gut–Brain Axis for Alzheimer’s Disease

“…Recently, a strong connection between inflammatory bowel disease and noncoding RNAs (ncRNAs) was also reported [ 43 ]. The potential use of immunonutritional vesicles (i.e., containing molecules to selectively drive TLR4-mediated responses and ncRNAs) could represent potential novel approaches for tackling aberrant CNS inflammation and microglia function [ 44 ].…”

“…Altogether, only in completion with their dynamics within the gastrointestinal tract can the functional features and bioactivities of the compounds be determined. To improve the bioavailability of immunometabolic neuroprotective compounds and thereby their effectiveness, making them useful in clinical practice, biocompatible vesicles as well as nanocarrier-based strategies could be used [ 44 , 131 ]. A better understanding of the interaction of those vehicles with human myeloid cells—including monocytes and macrophages derived from those—can help significantly improve phagocytic activity and functional polarization stimuli, favoring an anti-inflammatory peripheral profile of monocytes which can influence that of the microglia ( Figure 1 ).…”