Cell sources | Passage number | Influenza virus | Animal models | Other instructions | Biological effect |
---|---|---|---|---|---|
Human BM MSCs | Not reported | H5N1 | Mouse | 5×105 cells/mouse injected at 5 dpi | MSCs prevent or reduce virus associated ALI and increase likelihood of survival in the infected mouse [32]. |
Human UC MSCs | P4-5 | H5N1 | Mouse | 5×105 cells/mouse injected (i.v.) at 5 dpi | UC-MSCs increased the body weight ands lightly improved survival of the infected mice [34]. |
Mouse BM MSCs | P3-10 | H9N2 | Mouse | 5×105 cells/mouse injected (i.v.) at 30 mpi | MSCs treatment significantly reduces lung injury in mice and is associated with reduced pulmonary inflammation [33]. |
Swine BM MSCs derived Evs | P3-5 | H1N1/H7N2/H9N5 | Pig | 80μg/kg body weight injected(i.t.)at 12 hpi | MSC-EVs inhibited influenza virus replication and virus induced apoptosis in pig lung epithelial cells [35]. |
Human/murine BM MSCs | P3/P6-9 | H1N1 | Mouse | 2.5 or 5×105 cells/mouse injected (i.v.) at -2, 0, 2, 5 dpi | MSCs failed to improve survival, decrease pulmonary inflammatory cells or prevent ALI [41]. |
Human/murine BM MSCs | P7 or less | H1N1 | Mouse | 5×105 cells/mouse injected (i.v.) at 5/6 dpi | MSCs modestly reduced viral load andfailed to reduce the severity of influenza induced injury [42]. |
TPR63+/KRT5+ BCs | Â | H1N1 | Mouse | The endogenous lung cells | TPR63+/KRT5+ BCs initiate an injury repair process to keep normal lung function by differentiating into mature epithelium [46]. |
LNEP cells | Â | H1N1 | Mouse | The endogenous lung cells | LNEP cells can activate a TPR63+/KRT5+ remodeling program through Notch signaling [48]. |
KRT5- progenitor cells | Â | H1N1 | Mouse | The endogenous lung cells | The SOX2+/SCGB1A-/KRT5- progenitor cells can generate nascent KRT5+ cells [49]. A rare p63+Krt5- progenitor cell population also responds to H1N1 virus-induced severe injury [50]. |