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. Author manuscript; available in PMC: 2019 Aug 7.
Published in final edited form as: J Leukoc Biol. 2019 Feb 18;105(4):783–795. doi: 10.1002/JLB.4A1018-381R

FIGURE 2. HIV-1BaL infection induces an IL-1β response in primary CD68+ liver macrophages.

FIGURE 2

(A) Flow cytometry strategy to analyze IL-1β expression in isolated liver macrophages. (B) Flow cytometry analyses of IL-1β positive CD68+ macrophages directly before and after HIV-1BaL infection (n = 7; P = 0.031). (C) p24 was measured 48 hr postinfection with HIV-1BaL at an MOI of 0.10 (n = 8). (D) IL-1β mRNA (n = 8; P < 0.001), IFNα mRNA (n = 8; P = 0.105) and IFNβ mRNA (n = 8; P = 0.01) were measured by RT-PCR. (E) CD68+ liver macrophages were treated with HIV-1BaL, LPS, or LPS+HIV-1BaL and, IL-1β in culture supernatant was measured with ELISA (n = 15) HIV-1BaL vs. control, P = 0.008; LPS vs. control, P = 0.0003; LPS vs. LPS+ HIV-1BaL, P < 0.0001. (F) Cytotoxicity of control (n = 10), HIV-1BaL infected (n = 14), LPS treated (n = 4) or HIV-1BaL +LPS treated (n = 5) on isolated macrophages was examined by LDH assay to confirm that increases in IL-1β were not due to cell death (each sample quadruplicate). Panels B, D: Wilcoxon signed rank test; Panels E, F: Kruskal-Wallis one way analysis