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. Author manuscript; available in PMC: 2014 Mar 5.
Published in final edited form as: Nature. 2013 Aug 21;501(7465):52–57. doi: 10.1038/nature12479

Figure 3. Bacterial heat-stable components including N-formylated peptides activate nociceptors.

Figure 3

(a) Hk-S. aureus induces calcium flux in capsaicin, KCl responsive DRG neurons (arrows, traces). (b) (i) Representative recording, (ii) firing frequency upon hk-S. aureus application (5 capsaicin-responsive cells, 9 unresponsive). (c) DRG responsive proportions to hk-bacteria (n=4-26 fields/condition). (d) Acute pain induction: saline (n=13), hk-S. aureus (n=12), hk-S. pneumonia (n=14), hk-L. monocytogenes (n=5), hk-M. fermentans (n=6), hk-H. pylori (n=5), hk-P. aeruginosa (n=8), hk-E. coli (n=6). **p<0.01, *p<0.05. (e) DRG responsive proportions to formyl peptides (n=3-14 fields/condition). (f-g) fMLF, fMIFL injection induces mechanical hypersensitivity. Fpr1−/− mice show reduced hk-S. aureus mechanical hypersensitivity (p=0.0089). fMIFL vs. saline, Fpr1−/− vs. WT: *p<0.05; **p<0.01; ***p<0.001. Error bars, mean±s.e.m.