Fig. 7: ADH5 deficiency attenuates HSV-1- and L. monocytogenes-induced innate responses. | Nature Communications

Fig. 7: ADH5 deficiency attenuates HSV-1- and L. monocytogenes-induced innate responses.

From: S-nitrosothiol homeostasis maintained by ADH5 facilitates STING-dependent host defense against pathogens

Fig. 7

a–c qPCR analysis of Isg15, Isg54, Isg56, Mx1, HSV-1 UL30 mRNA expression and HSV-1 DNA level in HSV-1-infected PMs from Adh5+/+ or Adh5-/- mice. d Immunoblot assays of STING, p-TBK1, p-IRF3, and p-STAT1 in L. monocytogenes-infected PMs from Adh5+/+ or Adh5-/- mice. e ELISA analysis of IFN-β secretion in L. monocytogenes-infected PMs from Adh5+/+ or Adh5-/- mice. f–h qPCR analysis of Ifnb, Cxcl10, Isg15, Isg54, Isg56, and Mx1 mRNA expression in L. monocytogenes-infected PMs from Adh5+/+ or Adh5-/- mice. Data represent mean ± SD or one representative from three independent experiments. The p values were calculated using unpaired two-sided t test and adjustments were made for multiple comparisons.

Back to article page