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The edible mushroom Agaricus brasiliensis contains a large amount β-glucan, which is mainly composed of a β-1,6-glucan structure. In this study, we investigated the effect of A. brasiliensis strain KA21 on the anti-β-glucan antibody titer in healthy humans and the role of antibodies as an immunomodulator. Twenty-two healthy volunteers were fed the dried fruiting body of A. brasiliensis (900 or 1500 mg/day) for 12 weeks. The anti-β-glucan antibody titer in the serum was determined by enzyme-linked immunosorbent assay. Immunoglobulin G (IgG) against β-glucan was significantly upregulated after intake of A. brasiliensis. Murine experiments demonstrated improvement of anti-β-glucan antibody production after intraperitoneal injection of Agaricus-derived β-glucan. To understand the role of antibody against β-glucan in exclusion of pathogenic fungi, we examined the interaction between HL-60 cells and antibody-treated heat-killed Candida albicans. Flow cytometry analysis indicated the upregulation of Candida-positive HL-60 cells after treatment with human IgG, whereas the competitive assay demonstrated that the main epitope of Candida-reacted IgG was the β-1,6-glucan structure. Binding between HL-60 and IgG-opsonized C. albicans was suppressed by anti-Fcγ receptor 1 (FcγRI) neutralizing antibody. Finally, using FcγRI-expressed cells with the nuclear factor of activated T-cell reporter assay, we demonstrated that higher titers of anti-β-glucan IgG can induce stronger Fc receptor-mediated cell activation through the formation of an antibody-β-glucan complex. In conclusion, oral ingestion of A. brasiliensis KA21 promotes anti-β-glucan antibody production and may contribute to preventing fungal infection through the activation of immune cells by forming antibody-β-glucan complexes via an FcγR-dependent pathway.This review provides results obtained by scientists from different countries on the antiviral activity of medicinal mushrooms against influenza viruses that can cause pandemics. Currently, the search for antiviral compounds is relevant in connection with the coronavirus disease 2019 (COVID-19) pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Medicinal mushrooms contain biologically active compounds (polysaccharides, proteins, terpenes, melanins, etc.) that exhibit an antiviral effect. The authors present the work carried out at the State Research Center of Virology and Biotechnology Vector in Russia, whose mission is to protect the population from biological threats. The research center possesses a collection of numerous pathogenic viruses, which allowed screening of water extracts, polysaccharides, and melanins from fruit bodies and fungal cultures. The results of investigations on different subtypes of influenza virus are presented, and special attention is paid to Inonotus obliquus (chaga mushroom). Compounds produced from this mushroom are characterized by the widest range of antiviral activity. Comparative data are presented on the antiviral activity of melanin from natural I. obliquus and submerged biomass of an effective strain isolated in culture against the pandemic strain of influenza virus A/California/07/09 (H1N1 pdm09).Cerebral ischemia-reperfusion (CIR) is a common feature of ischemic stroke and is a major cause of disability and death among stroke patients worldwide. Phyllanthin, a lignin polyphenol, is known for its varied biological properties, although its protective effects against CIR have not been reported. We evaluated the neuroprotective property of phyllanthin against CIR as well as the involvement of the AMP-activated protein kinase/nuclear factor erythroid 2-related factor 2 (AMPK/Nrf2) and nuclear factor kappa B (NF-κB) signaling pathways. Experimental animals were divided into five groups controls (sham-operated), CIR-induced by middle cerebral artery occlusion (MCAO), and CIR-induced and administered phyllanthin at 2.5, 5, and 10 mg/kg, respectively. We investigated neurological functions, various signaling genes, and inflammatory clues. The results of in vitro assays demonstrated that phyllanthin assertively improved cellular functions through abrogation of the Nrf2 pathway. In vivo, CIR rats demonstrated neurological function deficits, while ischemic severity was evidenced by the activation of neuroinflammatory cytokines and tissue oxidative stress. Moreover, the expression of apoptosis markers such as Bax, B-cell lymphoma (Bcl-2), caspase-3, COX-2, PGE2, and LOX-1 abruptly increased. Phyllanthin prevented brain dysfunction and cerebral edema, and protected brain integrity. Conversely, it improved antioxidative enzyme activity, abrogated inflammatory cytokines, and increased IL-10 in chemokines. Also, phyllanthin significantly reduced Nrf2 and AMPK levels, with reduced expression of NF-κB indicating that cross-talk between the NF-kB and Nrf2 pathways is activated in CIR. Phyllanthin rescues the ischemic brain by regulating cellular signaling, which supports its use for complications like CIR and associated injury.Parkinson’s disease (PD) is the second most common neurodegenerative disease worldwide. Tomentosin is an active compound isolated from the I. viscosa plant that has extensive therapeutic value. In this exploration, the neuroprotective actions of tomentosin were investigated against MPTP-stimulated neuroinflammation in mice. JAK inhibitor PD was stimulated in C57/BL6 mice by injecting 20-mg/kg MPTP at 2-h intervals 4 times a day for 15 days simultaneously with tomentosin treatment. The rota-rod test, grasping test, and pole climbing test were executed to investigate the motor functioning of the test animals. Proinflammatory cytokines, reactive oxygen species, and myeloperoxidase were assayed using commercial ELISA kits. Superoxide dismutase enzyme levels were measured by the standard method. Expression of TLR-4/NF-κB was analyzed by Western blot. Brain tissues of investigational animals were analyzed microscopically. Tomentosin treatment of the MPTP-intoxicated PD mice promoted appreciable regains in body weight and noticeably prevented MPTP-stimulated impairments in motor function. In the PD mice, proinflammatory cytokine, ROS, and MPO levels were lowered by tomentosin, inhibited the TLR-4/NF-κB signaling pathway and prevented inflammation-mediated neuronal cell damage, and reduced glial cell damage and normalized ganglion layers. These findings confirmed the neuroprotective properties of tomentosin against MPTP-induced PD in mice.