PMC:7376974 / 77214-82867
Annnotations
{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7376974","sourcedb":"PMC","sourceid":"7376974","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7376974","text":"Innate Immune Response\nInnate immune response is the first response that takes place in the presence of any type of infection. During this early stage, interferon stimulating genes (ISGs) are upregulated in the infected cells.125 This self-defense mechanism slows down the viral replication and alerts sentinel immune cells that start producing proinflammatory cytokines and trigger inflammation.125 However, many viruses are able to escape this complex mechanism, retarding the immune response and spreading the infection. The interaction of HNMs with the immune system has been more and more studied. In the case of antiviral HNMs, many examples can be found in the literature where the NMs not only slow down the infection but also tune the innate immune response. Certain HMNs can display an intrinsic immune stimulation. We have already mentioned above that in the early stage of infection, AgNPs mainly prevent the virus from entering the host cell through the interaction with the external capsid, but in vitro cellular experiments lack to understand the complex interaction with primary immune cells. Recent studies have shown that AgNPs can potentially induce the expression of genes involved in innate and adaptive immunity-associated pathways, which are known to play crucial role in immune regulation. For example, Toll-like receptor 7 can be upregulated by AgNPs after 24 h, by recognizing the single-stranded RNA of the viruses and regulating the antiviral immune response.126 Another study showed that in RSV-infected mice treated with AgNPs, the particles reduced the production of pro-inflammatory TNF-α and IL-6 cytokines, but potentiated the anti-RSV activity of neutrophils in an experimental mouse model.127 However, activation of AgNPs in the reduction of RSV has been noted only when the NM was intranasally inoculated together with the virus, and no results have been reported on the use of AgNPs administrated on infected mice. In the case of influenza virus infection of lung epithelial cells, it was found that AgNPs targeted infected lung epithelial cells and reduced viral replication, by preventing autophagy. However, the blockage of the autophagic flux by AgNPs does not inhibit viral replication in already infected cells. Therefore, AgNPs are more suitable as viral preventive agents due to their pro-inflammatory response rather than drugs.128 More recently, AgNPs were combined with graphene materials and exploited as antiviral material for the treatment of Porcine reproductive and respiratory syndrome virus (PRRSV).129 GO-AgNPs were able to clump the virus diminishing its fusion with cell membrane. Additionally, once GO-AgNPs were internalized in host cells, they stimulated the ISGs that blocked viral budding and its diffusion to other cells in vitro (Figure 15).129\nFigure 15 Scheme of the mechanism of action of GO-AgNPs on activation of innate immunity. Reproduced with permission from ref (129). Copyright 2018 American Chemistry Society. Similarly, CDs used for the treatment of RSV and PRRSV were able to activate the innate immune response via an upregulation of ISGs in vitro.130 Gold nanorods were applied to boost the innate immune response against RSV in vivo.131 Interestingly, it was shown that these nanorods (when intranasally administered with RSV) were not only able to activate the ISGs but also to tune the production of pro- and anti-inflammatory cytokines, resulting in the blocking of the infection with a reduced pulmonary inflammation.131 As drug carriers, HNMs can also affect the internalization pathways, modulate drug efficacy, and the immune cell responses. For instance, it was found that the isoprinosine immunomodulatory antiviral drug displays a much higher antiviral efficacy in vivo when delivered with CNTs than as a pure drug (in zebrafish larvae food administration), probably due to a better cellular uptake and the anti-inflammatory properties of the nanotubes.132\nFullerenes also exhibit immunomodulation properties through the release of cytokines by bovine alveolar macrophages.133 A study explored the influence of functionalization of C60 with molecules presenting different surface charges like hydroxyl groups and amino acids.134 The study concluded that negative charges upregulated TNF-α up-secretion in RAW 264.7 macrophages, but highly positively or negatively charged surfaces increased cell toxicity. The upregulation of the cytokine TNF-α is a proof that fullerene can promote cellular immune response.\nDespite these preliminary results, the actual mechanisms of interaction between HNMs and the immune system are still at early stage of understanding. We must consider that the immune response needs to be proportional to the infection grade. If on one side nanosized immuno-boosters can alert more efficiently the sentinel cells, the use of HNMs that trigger an exaggerated immune response can promote excessive inflammation, damaging healthy cells and promoting uncontrolled side effects. In the particular context of SARS-Cov-2, the use of AgNPs, fullerenes, or other pro-inflammatory HNMs at the middle and late infection stage may cause an aggravation of the symptoms due to already diffused inflammation. In particular, most of the studies showed the ability to reduce infection when HNMs were first incubated with the pathogenic virus, thus limiting their potential use in the early stage infection.124 The formulation of HNMs able to both alert the immune system (e.g., upregulating cytokine) and control lung inflammation (e.g., ROS scavenger) even after the early stage infection may be a possible strategy for treatments against SARS 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