Abstract

Photodynamic inactivation of microorganisms (aPDI) is an excellent method to destroy antibiotic-resistant microbial isolates. The use of an exogenous photosensitizer or irradiation of microbial cells already equipped with endogenous photosensitizers makes aPDI a convenient tool for treating the infections whenever technical light delivery is possible. Currently, aPDI research carried out on a vast repertoire of depending on the photosensitizer used, the target microorganism, and the light delivery system shows efficacy mostly on in vitro models. The search for mechanisms underlying different responses to photodynamic inactivation of microorganisms is an essential issue in aPDI because one niche (e.g., infection site in a human body) may have bacterial subpopulations that will exhibit different susceptibility. Rapidly growing bacteria are probably more susceptible to aPDI than persister cells. Some subpopulations can produce more antioxidant enzymes or have better performance due to efficient efflux pumps. The ultimate goal was and still is to identify and characterize molecular features that drive the efficacy of antimicrobial photodynamic inactivation. To this end, we examined several genetic and biochemical characteristics, including the presence of individual genetic elements, protein activity, cell membrane content and its physical properties, the localization of the photosensitizer, with the result that some of them are important and others do not appear to play a crucial role in the process of aPDI. In the review, we would like to provide an overview of the factors studied so far in our group and others that contributed to the aPDI process at the cellular level. We want to challenge the question, is there a general pattern of molecular characterization of aPDI effectiveness? Or is it more likely that a photosensitizer-specific pattern of molecular characteristics of aPDI efficacy will occur?

Highlights

  • Antibacterial photodynamic inactivation is a therapeutic option used in the treatment of infectious diseases

  • The studies mentioned above demonstrate that Antibacterial photodynamic inactivation (aPDI)/antimicrobial blue light (aBL) treatment efficacy could be improved by controlling the DNA repair system, e.g., by inhibiting or eliminating the expression of the recA gene, and that recA is a critical element in the bacterial response to photoinactivation

  • We discuss several issues contributing to the various responses of bacteria to aPDI or aBL

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Summary

INTRODUCTION

Antibacterial photodynamic inactivation (aPDI) is a therapeutic option used in the treatment of infectious diseases It is based on a combination of a photosensitizer (PS), light and oxygen to remove highly metabolically active cells. The main element in aPDI is a triplet excited photosensitizer, whose action can lead to the formation of singlet oxygen and radicals, known as reactive oxygen species (ROS) [4]. The primary motivation for writing this review was to identify the molecular phenomena occurring in the cells of microorganisms during and after photosensitization that may influence the effectiveness of photodynamic inactivation and to identify the elements that determine the existence of microbial phenotypes with differences in vulnerability to aPDI. Despite the crucial role of the cell envelope in the bactericidal activity of photoinactivation, the actual contribution of DNA damage to the outcome of phototreatment should not be underestimated

PHOTOTREATMENT TOLERANCE
OXIDATIVE STRESS SENSING AND DETOXIFYING MECHANISMS
Oxidative Stress Elements Studied With Respect to aPDI
KEY MASTER REGULATOR OF STRESS RESPONSE
DNA REPAIR ENZYMES
Role of LexA in Phototreatment Outcome
HETEROGENOUS RESPONSE TO APDI AND GENETIC BACKGROUND
Lipid Composition of Bacterial Membranes
The Role of Bacterial Pigments in aPDI
PHOTOSENSITIZER ACCUMULATION IN CELLS
CONCLUSIONS
Findings
AUTHOR CONTRIBUTIONS
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