From: Exosome-mediated regulation of inflammatory pathway during respiratory viral disease
Virus | Exosome source | Exosome cargo | Sample (in vitro, in vivo) | Induction or inhibition of inflammation | Note | References |
---|---|---|---|---|---|---|
Respiratory syncytial viruses | RSV-infected A549 cells | – | In vitro (RSV-infected A549 cells) | Induction | Exosomes derived from RSV-infected A549 cells secrete significantly higher levels of RANTES, IP-10, and TNF-α, which activate the innate immune response and may through the release of pro-inflammatory cytokines and apoptosis in receptor cells have antiviral effects | [101] |
Influenza | Respiratory epithelial cell lines | NP, NS1, M1, HA | In vitro (Respiratory epithelial cell lines) | Inhibition | Exosomes derived from respiratory epithelial cell lines infected with influenza virus showed an anti-viral response, which may inhibit inflammation in the early stages | [106] |
Influenza | Bronchial alveolar lavage fluid (BALf) of influenza virus | – | In vitro (bronchial alveolar lavage fluid (BALf) of influenza virus) | Induction | Exosomes derived from bronchial alveolar lavage fluid (BALf) of influenza virus produce IL-6, MCP-1, and TNF, which are inflammatory cytokines and increase inflammation | [106] |
Influenza | Macrophages, fibroblasts, T cell, and B cell lines | Nucleoprotein (NP) and non-structural protein (NS1) | In vitro (macrophages, fibroblasts, T cell, and B cell lines) | Induction | Levels of pro-inflammatory cytokines, such as IFN-γ, IL-1β, and CXCL8, were also elevated by the exosomes | [136] |
Influenza | Bronchoalveolar lavage fluid (BALF) | miR-483-3p | In vitro (bronchoalveolar lavage fluid (BALF)) | Induction | The transfer of miR-483-3p from bronchoalveolar lavage fluid (BALF) caused the expression of type I interferon and proinflammatory cytokine genes and strengthened their face | [137] |
Influenza | Exosomes derived from H5N1-infected chickens | Viral proteins, NP and NS1 | In vitro (exosomes derived from H5N1-infected chickens) | Induction | The presence of viral proteins such as NP and NS1 in exosomes derived from H5N1-infected chickens increases the level of pro-inflammatory cytokines such as IFN-γ, IL-1β, and IL-8 | [119] |
Influenza | Bronchoalveolar lavage fluid (BALF) | miR-483-3p, miR-374c-5p, miR-466i-5p, miR-203-3p | In vitro (bronchoalveolar lavage fluid (BALF)) | Induction | miR-483-3p, miR-374c-5p, miR-466i-5p, miR-203-3p in exosomes derived from bronchoalveolar lavage fluid (BALF) significantly increased IFN-β expression, proinflammatory cytokine gene expression, and upregulates interferon-stimulated genes (ISGs), including IL6, CCL2, TNF-α, and SP110 | [138] |
Parainfluenza | Madin–Darby bovine kidney (MDBK) cells inoculated with CPIV3 | miRNA 11 | In vitro (Madin–Darby bovine kidney (MDBK) cells inoculated with CPIV3) | Unknown | These exosomes could transfer CPIV3 genetic materials to recipient cells to establish a productive infection and promote viral replication | [139] |
Rhinoviruses | Primary bone marrow-derived DCs (BMDCs) | MiR155 | in vitro and in vivo | Induction | miR-155 in exosomes derived from primary bone marrow-derived DCs (BMDCs) is essential for Th2-mediated eosinophilic inflammation in the lung and induces inflammatory conditions in the body | [118] |
Rhinoviruses | RV-infected AECs | – | In vitro | Induction | Exosomes from RV-infected AECs yielded significant inflammatory cytokines/chemokines such as CXCL8, which induced an inflammatory state in the body | [140] |
Rhinoviruses | Bronchoalveolar lavage fluid | – | In vitro | Induction | – | [141] |
Coronaviruses | Lung macrophages | Nsp12 and Nsp13 | In vitro | Induction | Nsp12 and Nsp13 in exosomes derived from lung macrophages lead to the activation of nuclear factor κB (NF-κB) and subsequent induction of an array of inflammatory cytokines | [127] |
Coronaviruses | Patient plasma | Tenascin-C (TNC) and fibrinogen-β (FGB) | In vitro | Induction | Tenascin-C (TNC) and fibrinogen-β (FGB) induce the production of pro-inflammatory cytokines through interaction with the NF-κB inflammatory signaling pathway. FGB is transported via plasma exosomes and potentially induces pro-inflammatory cytokine signals in distant organ cells | [128] |
Coronaviruses | A549 cell | Viral protein E, Nsp7, Nsp10, Nsp12, Nsp13, and slight protein M | In vitro | Induction | The RNA polymerase, Nsp12, alone inhibits tumor necrosis factor (TNF)-α and interleukin (IL)-6. Furthermore, a synergistic effect of Nsp12 working with Nsp13 was observed where, compared to Nsp12 alone, there was a significant induction of TNF-α, IL-1β, and IL-6, which are inflammatory cytokines. In contrast, M protein, Nsp13 alone, or Nsp10 did not | [127] |
Coronaviruses | Endothelial cells | – | In vitro | Induction | Exosomes derived from endothelial cells infected with coronaviruses lead to NLRP3 inflammasome activation in endothelial cells of distant organs, which ultimately leads to IL-1β secretion and inflammatory response | [128] |
Adenoviruses | Bone marrow-derived dendritic cells (DCs) | Expressing viral IL-10 | In vitro | Inhibition | Â | [142] |
Adenoviruses | Derived from FasL-expressing DC | – | In vitro | Inhibition | Mice are immunized with a specific antigen, keyhole limpet hemocyanin (KLH). Then a Th1-mediated inflammatory response is induced 10 to 14 days after immunization by injection of the particular antigen into the hind pads. Mice immunized with KLH 106 DC or 1 μg exosome received in one hind paw 12 h before KLH booster injection into both hind paws. Delivery of DC/FasL or DC/FasL-derived exosomes significantly reduced paw swelling not only in the treated paw but also in the contralateral paw. Untreated suppressed 24, 48, and 72 h after antigen injection. These results show that genetically modified DC-expressing FasL as well as DC/FasL-derived exosomes are equally effective in suppressing the DTH response not only in the treated paw, but they are also in the untreated opposite paw | [135] |
Adenovirus | Infected A549 | – | In vitro | Induction | A549-derived exosomes infected with adenoviruses significantly increased IL-1β protein, which induced inflammatory conditions in the body | [134] |