Technical CommentsSepsis

Response to comment on “ALK is a therapeutic target for lethal sepsis”

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Science Translational Medicine  12 Dec 2018:
Vol. 10, Issue 471, eaas9817
DOI: 10.1126/scitranslmed.aas9817

Figures

  • Fig. 1 Knockout of ALK limits STING activation in macrophages.

    (A) Western blot analysis of ALK expression in isolated peritoneal macrophages from septic Alk+/+ or Alk−/− mice at 48 hours after cecal ligation and puncture (CLP). (B and C) Analysis of IFN-β mRNA (B) and release (C) in Alk+/+ or Alk−/− peritoneal macrophages with or without indicated STING ligand (10 μg/ml) stimulation for 16 hours (n = 3, *P < 0.05). (D) Confocal microscope imaging analysis of colocalization between ALK (green) and F4/80 (red) in lung from CLP-induced septic mice at 48 hours. (E) Confocal microscope imaging analysis of colocalization between ALK (green) and F4/80 (red) in lung tumor from a patient with NSCLC. Hoechst 33258 (blue) was used for nuclear staining. AU, arbitrary units.

  • Fig. 2 ALK depletion protects mice against CLP-induced polymicrobial sepsis.

    (A) Depletion of ALK in mice prevented CLP (22-gauge needle)–induced animal death (n = 8 mice per group; *P < 0.05, Kaplan-Meier survival analysis). (B) In parallel, indicated serum enzyme activity (day 3) was assayed (n = 5 mice per group; *P < 0.05). CK, creatinine kinase; AMYL, amylase; BUN; blood urea nitrogen; ALT, alanine aminotransferase.

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