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. Author manuscript; available in PMC: 2022 Dec 7.
Published in final edited form as: Cell Metab. 2021 Oct 27;33(12):2428–2444.e8. doi: 10.1016/j.cmet.2021.10.003

Figure 2: Activation Strength of Intra-muscular NF-kB/Innate Immune Signaling Directs Re-allocation of Host Energy Substrates to Alter Host-Pathogen Susceptibility.

Figure 2:

(A-B) Induction of Dro-GFP after P.e. oral infection in (A) Dro-GFP flies, (B) control flies (w1118; Dro-GFP; Act88FGal4) or flies with muscle-specific attenuation of the NF-kB innate immune pathway (w1118; Dro-GFP; Act88FGal4>UAS-RelishRNAi#1 or UAS-PGRP-LERNAi).

(C-G) Changes in systemic lipid metabolism in Act88FGal4>UAS-RelishRNAi#1 or UAS-PGRP-LERNAi or UAS-PGRP-LCRNAi flies after P.e. oral infection. (C and G) Neutral lipid ORO stain and (C) Nile-red stain of dissected carcass/fat body. (D-E) Total TAG levels of whole flies after infection at 8hrs (D) and 20hrs (E); n=4. (F) Circulating lipids levels from isolated hemolymph; n=3.

(H-M) Infection outcomes in Act88FGal4>UAS-RelishRNAi#1 or UAS-PGRP-LERNAi flies after P.e. oral infection. (H-I) Measurement of CFUs (8hrs or 20hrs); n=10. (J-K) Measurement of defecation; n=200. (L-M) Survival rates; n=200.

(N-O) Measurement of fecundity (egg laying) of (N) Act88FGal4>UAS-RelishRNAi#1 flies and (O) Dro-GFP flies after (during) or post P.e. oral infection.

Error bars represent mean±SE, *P<0.01.