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Analysis of the Bacterial Heat Shock Response to Photodynamic Therapy‐mediated Oxidative Stress
Author(s) -
St. Denis Tyler G.,
Huang Liyi,
Dai Tianhong,
Hamblin Michael R.
Publication year - 2011
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.2011.00902.x
Subject(s) - enterococcus faecalis , photosensitizer , heat shock protein , photodynamic therapy , escherichia coli , microbiology and biotechnology , groel , bacteria , heat shock , antimicrobial , chemistry , hsp70 , biology , biochemistry , photochemistry , genetics , organic chemistry , gene
Antimicrobial photodynamic therapy (PDT) has recently emerged as an effective modality for the selective destruction of bacteria and other pathogenic microorganisms. We investigated whether PDT induced protective responses such as heat shock proteins (HSPs) in bacteria. Using the photosensitizer Toluidine Blue O (TBO) at sublethal PDT conditions, a seven‐fold increase in bacterial HSP GroEL and a three‐fold increase in HSP DnaK were observed in Escherichia coli post PDT. Pretreatment with 50°C heat for 30 min reduced PDT killing in both E. coli and in Enterococcus faecalis , with the most pronounced inhibition occurring at 50 μ m TBO with 5 J cm −2 635 nm light, where E. coli killing was reduced by 2 log 10 and E. faecalis killing was reduced by 4 log 10 . Finally, inhibition of the highly conserved chaperone DnaK using a small molecule benzylidene lactam HSP inhibitor potentiated (but not significantly) the effect of PDT at a TBO concentration of 2.5 μ m in E. faecalis ; however, this effect was not observed in E. coli presumably because inhibitor could not gain access due to Gram‐negative permeability barrier. Induction of HSPs may be a mechanism whereby bacteria could become resistant to PDT and warrants the need for further study in the application of dual PDT‐HSP‐inhibition therapies.