Fig. 5: Autophagy dysregulation in glial cells induced by HSV-1 infection on the NVU model. | Nature Communications

Fig. 5: Autophagy dysregulation in glial cells induced by HSV-1 infection on the NVU model.

From: A microengineered 3D human neurovascular unit model to probe the neuropathogenesis of herpes simplex encephalitis

Fig. 5

a KEGG pathway enrichment analysis of upregulated genes and downregulated genes in astrocytes following HSV-1 infection at 3 dpi. b KEGG pathway enrichment analysis of upregulated genes and downregulated genes in microglia following HSV-1 infection at 3 dpi. a, b Autophagy-related terms were marked with red boxes. The analyses were all one-sided and adjustments were made for multiple comparisons. c TEM images showing microglia on Mock or HSV-1-infected NVU models at 3 dpi (n = 3 for biological replicates; n = 3 for technical replicates). The autophagic vacuoles were indicated by red asterisks. d Confocal micrographs showing the microglia immunostained for p62 (green) and LC3B (red) following HSV-1 infection at 3 dpi on the chip (n = 3 for biological replicates; n = 3 for technical replicates). The chip treated with rapamycin was used as a positive control group. e Confocal micrographs showing autophagic flux in microglia following HSV-1 infection at 3 dpi (n = 3 for biological replicates; n = 3 for technical replicates). The red dots indicate autolysosome, and the yellow dots indicate autophagosome. The chip treated with rapamycin was used as a positive control. f Quantification of autolysosome and autophagosome numbers in microglia following HSV-1 infection based on (e) (n = 3 for biological replicates; n = 3 for technical replicates). Ten cells were quantified for each chip. Data are presented as the mean ± SD and were analyzed using an unpaired two-sided Student’s t-test.

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