Dermatological and cosmetics fields have recently started to focus on the human skin microbiome and microbiota, since the skin microbiota is involved in the health and dysbiosis of the skin ecosystem. Amongst the skin microorganisms, Staphylococcus epidermidis and Cutibacterium acnes, both commensal bacteria, appear as skin microbiota sentinels. These sentinels have a key role in the skin ecosystem since they protect and prevent microbiota disequilibrium by fighting pathogens and participate in skin homeostasis through the production of beneficial bacterial metabolites. These bacteria adapt to changing skin microenvironments and can shift to being opportunistic pathogens, forming biofilms, and thus are involved in common skin dysbiosis, such as acne or atopic dermatitis. The current evaluation methods for cosmetic active ingredient development are discussed targeting these two sentinels with their assets and limits. After identification of these objectives, research of the active cosmetic ingredients and products that maintain and promote these commensal metabolisms, or reduce their pathogenic forms, are now the new challenges of the skincare industry in correlation with the constant development of adapted evaluation methods.

Many studies performed in the last decade have focused on the cutaneous microbiota. It has been shown that this microbiota plays a key role in skin homeostasis. Considered as “a second barrier” to the environment, it is very important to know how it reacts to exogenous aggressions. The cosmetics industry has a started to use this microbiota as a source of natural ingredients, particularly ones that confer photoprotection against ultraviolet (UV) rays. Interestingly, it has been demonstrated that bacterial molecules can block UV rays or reverse their harmful effects. Oral probiotics containing living microorganisms have also shown promising results in restoring skin homeostasis and reversing the negative effects of UV rays. Microbial-based active sunscreen compounds have huge potential for use as next-generation photoprotection products.

The pioneering work of Kaplan and Greenberg [1] led to admit that, as eukaryotic cells, bacteria can communicate. In fact, many multicellular social bacterial behaviours such as swarming type motility, [2] biofilm formation [3] and virulence expression, [4] require population synchronization and that is performed at least partly through a highly regulated cell-to-cell communication system called quorum sensing (QS). QS is based on the bacterial population density, which is performed through secretion and sensing of specific signal molecules named autoinducers. Nowadays, many QS autoinducers, such as the N-acyl homoserine lactones (AHL) and quinolones (Gram-negative

Bacteria are frequently exposed to endogenous and exogenous reactive oxygen and nitrogen species which can damage various biomolecules such as DNA, lipids, and proteins. High concentrations of these molecules can induce oxidative and nitrosative stresses in the cell. Reactive oxygen and nitrogen species are notably used as a tool by prokaryotes and eukaryotes to eradicate concurrent species or to protect themselves against pathogens. The main example is mammalian macrophages that liberate high quantities of reactive species to kill internalized bacterial pathogens. As a result, resistance to these stresses is determinant for the survival of bacteria, both in the environment and in a host. The first bacterial component in contact with exogenous molecules is the envelope. In Gram-negative bacteria, this envelope is composed of two membranes and a layer of peptidoglycan lodged between them. Several mechanisms protecting against oxidative and nitrosative stresses are present in the envelope, highlighting the importance for the cell to deal with reactive species in this compartment. This review aims to provide a comprehensive view of the challenges posed by oxidative and nitrosative stresses to the Gram-negative bacterial envelope and the mechanisms put in place in this compartment to prevent and repair the damages they can cause.

The skin constitutes with its microbiota the first line of body defense against exogenous stress including air pollution. Especially in urban or sub-urban areas, it is continuously exposed to many environmental pollutants including gaseous nitrogen dioxide (gNO2). Nowadays, it is well established that air pollution has major effects on the human skin, inducing various diseases often associated with microbial dysbiosis. However, very few is known about the impact of pollutants on skin microbiota. In this study, a new approach was adopted, by considering the alteration of the cutaneous microbiota by air pollutants as an indirect action of the harmful molecules on the skin. The effects of gNO2 on this bacterial skin microbiota was investigated using a device developed to mimic the real-life contact of the gNO2 with bacteria on the surface of the skin. Five strains of human skin commensal bacteria were considered, namely Staphylococcus aureus MFP03, Staphylococcus epidermidis MFP04, Staphylococcus capitis MFP08, Pseudomonas fluorescens MFP05, and Corynebacterium tuberculostearicum CIP102622. Bacteria were exposed to high concentration of gNO2 (10 or 80 ppm) over a short period of 2 h inside the gas exposure device. The physiological, morphological, and molecular responses of the bacteria after the gas exposure were assessed and compared between the different strains and the two gNO2 concentrations. A highly significant deleterious effect of gNO2 was highlighted, particularly for S. capitis MFP08 and C. tuberculostearicum CIP102622, while S. aureus MFP03 seems to be the less sensitive strain. It appeared that the impact of this nitrosative stress differs according to the bacterial species and the gNO2 concentration. Thus the exposition to gNO2 as an air pollutant could contribute to dysbiosis, which would affect skin homeostasis. The response of the microbiota to the nitrosative stress could be involved in some pathologies such as atopic dermatitis.

Anthropogenic atmospheric pollution and immune response regularly expose bacteria to toxic nitrogen oxides such as NO• and NO2. These reactive molecules can damage a wide variety of biomolecules such as DNA, proteins and lipids. Several components of the bacterial envelope are susceptible to be damaged by reactive nitrogen species. Furthermore, the hydrophobic core of the membranes favors the reactivity of nitrogen oxides with other molecules, making membranes an important factor in the chemistry of nitrosative stress. Since bacteria are often exposed to endogenous or exogenous nitrogen oxides, they have acquired protection mechanisms against the deleterious effects of these molecules. By exposing bacteria to gaseous NO2, this work aims to analyze the physiological effects of NO2 on the cell envelope of the airborne bacterium Pseudomonas fluorescens MFAF76a and its potential adaptive responses. Electron microscopy showed that exposure to NO2 leads to morphological alterations of the cell envelope. Furthermore, the proteomic profiling data revealed that these cell envelope alterations might be partly explained by modifications of the synthesis pathways of multiple cell envelope components, such as peptidoglycan, lipid A, and phospholipids. Together these results provide important insights into the potential adaptive responses to NO2 exposure in P. fluorescens MFAF76a needing further investigations.

In the environment, microorganisms are subjected to a wide range of stresses. These stresses can be of natural origin, like temperature variations and ultraviolet exposure, but can also originate from humans like air pollution. The effects of air pollution on humans are more and more studied and reveal increasing concerns for human health, including augmentations of respiratory infections. However, the microbial responses to atmospheric pollution are still largely unknown. In a similar fashion, few studies investigate the effects of UV radiation on microorganisms. As NO2 is an air pollutant causing nitrosative stress in biological organisms by reacting with various biological molecules, solar UV radiations are also an important environmental source of cell damage. UVB can directly damage DNA and cause erythema, but only represent 6% of the total UV reaching the earth surface. The 94% others are UVA, that cause oxidative stress in the cells. Since oxidative and nitrosative stresses are interlinked, the exposition of airborne bacteria to these two stresses could have synergistic consequences. In this study, the airborne Pseudomonas fluorescens strain MFAF76a was exposed successively to gaseous NO2 and UV light to assess whether these two environmental stresses have synergistic effects on bacterial physiology. Bacterial growth was assessed by optical density and membrane permeability by flow cytometry. Exposures to successively gaseous NO2 and UVB light lead to a non-synergistic decrease of bacterial viability. Furthermore, only NO2 seems to damage the membrane and induces membrane permeabilization. Lipidomic analysis reveals similarities between the lipidic profile of bacteria in their exponential growth phase or for the exposed ones to NO2 during their stationary growth phase. Furthermore, lipidic alterations show that mechanisms induced by NO2 differ from those implemented by temperature. In conclusion, this study reveals that bacterial alterations caused by NO2 are specific, with a strong emphasis on membrane damage.

We report the draft genome sequences of two Micrococcus luteus strains, MFP06 and MFP07, isolated from human skin. The genome assemblies consist of 2,480 and 2,417 kbp with 2,337 and 2,240 coding sequences, respectively. The genomes contain genes potentially involved in osmotic stress tolerance, DNA repair, monoacylglycerol hydrolysis, and beta-lactone synthesis.