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. 2022 May 17;298(6):102036. doi: 10.1016/j.jbc.2022.102036

Figure 1.

Figure 1

Infection with Porphyromonas gingivalis leads to activation of SGK1 in innate immune cells. Primary human monocytes (A), BMDMs (B), and primary mice keratinocytes (C) were stimulated with P. gingivalis 33277 (Pg), Streptococcus gordonii DL1 (Sg), or Streptococcus sanguinis (Ss) at MOI of 10, for the time indicated. The whole cell lysates were collected for Western blotting, and the immunoblots were probed for phosphorylation and total expression of SGK1 and its prototypical substrate, NDRG1, in human monocytes (A), BMDMs (B), and primary keratinocytes (C), respectively. D–F, the intensity ratios of phosphorylation of SGK1 or NDRG1 relative to total SGK1 or NDRG1 for human monocytes (D), BMDMs (E), and primary keratinocytes (F) were determined by densitometry quantification assay. All the blots shown are representative of 3 to 5 independent experiments. BMDM, bone marrow–derived macrophage; MOI, multiplicity of infection; NDRG1, N-myc downstream–regulated gene 1; SGK1, serum- and glucocorticoid-regulated kinase 1.