Electricity-producing Staphylococcus epidermidis counteracts Cutibacterium acnes

Abstract Staphylococcus epidermidis (S. epidermidis) ATCC 12228 was incubated with 2% polyethylene glycol (PEG)-8 Laurate to yield electricity which was measured by a voltage difference between electrodes. Production of electron was validated by a Ferrozine assay. The anti-Cutibacterium acnes (C. acnes) activity of electrogenic S. epidermidis was assessed in vitro and in vivo. The voltage change (~ 4.4 mV) reached a peak 60 min after pipetting S. epidermidis plus 2% PEG-8 Laurate onto anodes. The electricity produced by S. epidermidis caused significant growth attenuation and cell lysis of C. acnes. Intradermal injection of C. acnes and S. epidermidis plus PEG-8 Laurate into the mouse ear considerably suppressed the growth of C. acnes. This suppressive effect was noticeably reversed when cyclophilin A of S. epidermidis was inhibited, indicating the essential role of cyclophilin A in electricity production of S. epidermidis against C. acnes. In summary, we demonstrate for the first time that skin S. epidermidis, in the presence of PEG-8 Laurate, can mediate cyclophilin A to elicit an electrical current that has anti-C. acnes effects. Electricity generated by S. epidermidis may confer immediate innate immunity in acne lesions to rein in the overgrowth of C. acnes at the onset of acne vulgaris

Associations with metabolites in Chinese suggest new metabolic roles in Alzheimer's and Parkinson's diseases

10.1093/hmg/ddz246HUMAN MOLECULAR GENETICS292189-20

Discovery of indolylpiperazinylpyrimidines with dual-target profiles at adenosine A_2A and dopamine D₂ receptors for Parkinson's disease treatment - Fig 5

<p>Dose-response curves of compound <b>5</b> (A), compound <b>6</b> (B) and (±)-PPHT.HCl (C) in D₂R-proteopolymersomes-based fluorescence polarisation (FP) competition assay with BODIPY-NAPS. The non-binding control (D) was achieved by denaturing the D₂R-proteopolymersomes with heat, resulting in a curve that fluorescence intensity did not decrease much when the concentration of (±)-PPHT.HCl increased. For the highest concentrations, experiments were repeated only in duplicate due to solubility issues.</p

Binding affinity (<i>K</i>_i, μM) of compounds 5–25 at human adenosine receptor subtypes.

<p>Binding affinity (<i>K</i>_i, μM) of compounds 5–25 at human adenosine receptor subtypes.</p

Structures of L-DOPA, KW-6002 and quinpirole.

<p>Structures of L-DOPA, KW-6002 and quinpirole.</p

Discovery of indolylpiperazinylpyrimidines with dual-target profiles at adenosine A_2A and dopamine D₂ receptors for Parkinson's disease treatment - Fig 5

<p>Dose-response curves of compound <b>5</b> (A), compound <b>6</b> (B) and (±)-PPHT.HCl (C) in D₂R-proteopolymersomes-based fluorescence polarisation (FP) competition assay with BODIPY-NAPS. The non-binding control (D) was achieved by denaturing the D₂R-proteopolymersomes with heat, resulting in a curve that fluorescence intensity did not decrease much when the concentration of (±)-PPHT.HCl increased. For the highest concentrations, experiments were repeated only in duplicate due to solubility issues.</p

Flowchart of virtual screening.

<p>The data are also extrapolated from <b><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0188212#pone.0188212.s005" target="_blank">S2</a>–<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0188212#pone.0188212.s011" target="_blank">S8</a> Figs</b>.</p

Inhibition of cAMP accumulation induced by compound 6 in comparison with the reference compound quinpirole (Q).

<p>The CHO cells were transfected with D₂ receptor, pre-treated with the indicated concentrations of quinpirole or compound <b>6</b>, and activated with forskolin/IBMX. (A) The cAMP concentration (in the unit of picomole) measured by ELISA. (B) Normalisation to control (0%) and 1 μM quinpirole (100%). *p<0.05. Error bars = standard error of the mean (SEM).</p