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. 2016 Dec 8;215(3):456–465. doi: 10.1093/infdis/jiw569

Figure 3.

Figure 3.

A, Images of Western blot analysis of hexokinase II expression during Chlamydia infection. Ten μg total protein from C57epi cells uninfected/infected with C. muridarum (MoPn) for 48 hours and treated/nontreated with inhibitor of PERK kinase activity were prepared for Western blot analysis. Blot was probed with primary antibody against hexokinase II. Lane 1: protein molecular weight marker. Lane 2: sample from noninfected C57epi cells at 48 hours. Lane 3: sample from C57epi cells infected with MoPn at MOI 5 for 48 hours. Lane 4: sample from C57epi cells infected with MoPn at MOI 5 in the presence of inhibitor of PERK kinase activity for 48 hours. B, Images of Western blot analysis of Glut1 and hexokinase II expression during Chlamydia infection. C57epi cells infected with C. muridarum (MoPn) induced the upregulation of key proteins in the IRE1α arm of UPR pathways, including Glut1 and hexokinase II, and the inhibition of IRE1α RNase activity, resulting in their downregulation. Ten μg total protein from C57epi cells uninfected/infected with C. muridarum for 48 hours and treated/nontreated with inhibitor of IRE1α RNase activity were prepared for Western blot analysis. Blot was probed with primary antibody against Glut1 or hexokinase II. Lane 1: protein molecular weight marker. Lane 2 sample from noninfected C57epi cells at 48 hours. Lane 3: sample from C57epi cells infected with MoPn at MOI 5 for 48 hours. Lane 4: sample from C57epi cells infected with MoPn at MOI 5 in the presence of inhibitor of IRE1α RNase activity for 48 hours. Abbreviations: C57epi cells, mouse oviduct epithelial cells; Glut1, glucose transporter-1; IRE1α, inositol-requiring enzyme-1α; MOI, multiplicity of infection; MoPn, mouse pneumonitis; NI, noninfected; PERK, protein kinase RNA-activated–like ER kinase; RNase, ribonuclease; UPR, unfolded protein response.