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. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: Innate Immun. 2016 Nov 24;23(2):111–127. doi: 10.1177/1753425916679255

Figure 2.

Figure 2

Live C. burnetii accumulates in the intestinal lumen of C. elegans and generates overt pathologies. Wild type C. elegans populations were separately exposed to live, mCherry-expressing- E. coli (CEC) or C. burnetii (CCB) as lawns on the surface of NNGM, and examined by fluorescence microscopy after 4 d of exposure. (a, b) Nematodes fed live CEC consistently showed that C. elegans was capable of digesting live E. coli. (c, d) In contrast, nematodes fed live CCB exhibited an intense mCherry signal that appeared to be restricted to the intestinal lumen. Accumulation of C. burnetii in C. elegans led to a swollen intestinal lumen and Dar that were not observed in worms fed (a) live E. coli or dead C. burnetii (not shown). Images were acquired at the same exposure time and joined and oriented with worm anteriors at the top. Bar =50 μM. BC: buccal cavity; Ph: pharynx; PIV: pharyngeal–intestinal valve; Mi: midgut; Hi: hindgut; An: anus; IL: intestinal lumen; PC: phase contrast; mCh: fluorescent mCherry signal.