Cancer vaccines based on resected tumors from patients have gained great interest as an individualized cancer treatment strategy. However, eliciting a robust therapeutic effect with personalized vaccines remains a challenge because of the weak immunogenicity of autologous tumor antigens. Utilizing exogenous prokaryotic constituents that act as adjuvants to enhance immunogenicity is a promising strategy to overcome this limitation. However, nonspecific stimulation of the immune system may elicit an undesirable immunopathological state. To specifically trigger sufficient antitumor reactivity without notable adverse effects, we developed an antigen and adjuvant codelivery nanoparticle vaccine based on Escherichia coli cytoplasmic membranes (EMs) and tumor cell membranes (TMs) from resected autologous tumor tissue. Introduction of the EM into the hybrid membrane nanoparticle vaccines (HM-NPs) induced dendritic cell maturation, thus activating splenic T cells. HM-NPs showed efficacy in immunogenic CT26 colon and 4T1 breast tumor mouse models and also efficiently induced tumor regression in B16-F10 melanoma and EMT6 breast tumor mouse models. Furthermore, HM-NPs provoked a strong tumor-specific immune response, which not only extended postoperative animal survival but also conferred long-term protection (up to 3 months) against tumor rechallenge in a CT26 colon tumor mouse model. Specific depletion of different immune cell populations revealed that CD8+ T and NK cells were crucial to the vaccine-elicited tumor regression. Individualized autologous tumor antigen vaccines based on effective activation of the innate immune system by bacterial cytoplasmic membranes hold great potential for personalized treatment of postoperative patients with cancer.

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Background and Aim Inflammatory bowel disease results from a dysregulated immune response to intestinal microbial flora in individuals with genetic predisposition(s). This study aimed to determine the effects of compound polysaccharides (CP) containing yam polysaccharide and inulin on the rat model of colitis induced by 2,4,6‐trinitrobenzenesulfonic acid (TNBS) and to explain the mechanism in terms of gut microbiota composition and function. Methods Male SD rats were divided into three groups: the control group, the model group, and the CP group. Disease activity index, serum myeloperoxidase level, and the composition and function of gut microbiota were analyzed. Results The data in the study showed CP reduced inflammation in the rat model of colitis induced by TNBS and ameliorated the experimental colitis. The results also indicated that CP not only reversed TNBS‐induced gut dysbiosis‐indexed by increased short‐chain fatty acids (SCFAs)‐producing bacteria, lactic acid‐producing bacteria, and decreased Bacteroides, Proteobacteria as well as sulfate‐reducing bacteria, but also restored the dysregulated microbiota function of colitic rats into a normal condition, including an improvement on basic metabolism and a reduction on oxidative stress, cell motility, signal transduction, xenobiotics biodegradation, and metabolism as well as pathogenesis processes. Conclusions Compound polysaccharides ameliorated the experimental colitis of rats induced by TNBS by modulating the gut microbiota composition and function profiles, which makes it possible to be used as prebiotic agents to treat gut dysbiosis in colitis individuals.

Systemic chemotherapy for treating tumors often leads to serious systemic side effects and affects patient compliance. Although the emerging technology of drug delivery systems (DDSs) can deliver the required cargo to tumor sites, DDSs are limited due to insufficient targeting ability or deficient pharmacokinetics. Herein, we assembled a novel targeting DDS for precision tumor therapy by applying a tumor-targeting polypeptide cyclic RGD (cRGD)modified erythrocyte membrane (eM-cRGD) cloaked on zeolitic imidazolate framework-8 (ZIF-8) nanoparticles (NPs) with encapsulated doxorubicin (DOX). For a mass ratio of ZIF-8:DOX = 1:1, the loading capacity was up to 49%. The nanoscale-sized targeting DDS promoted NP accumulation in tumor tissues via enhanced permeability and retention (EPR) effects, and the NPs actively targeted ligands and were then transferred to endosomes. The pH-sensitive carriers released higher DOX levels under the low pH mimicking that of a tumor microenvironment and tumor intracellular organelles, allowing enhanced inhibition of cancer cell growth.