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.

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.

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 NO₂on the cell envelope of the airborne bacteriumPseudomonas fluorescensMFAF76a and its potential adaptive responses. Electron microscopy showed that exposure to NO₂leads 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 NO₂exposure inP. fluorescensMFAF76a needing further investigations.

We previously showed that the physiological concentration of 17β-estradiol in the vaginal environment is sufficient to affect the membrane dynamics and adhesion phenotype of the Lactobacillus crispatus strain CIP104459. However, L. crispatus is a heterogeneous species. Here, we investigated the effect of 17β-estradiol on the recently isolated L. crispatus vaginal strain V4, related to a cluster distant from CIP104459 and at the limit of being a different subspecies. Grown in the same medium, the two strains expressed a highly similar pool of proteins. However, in contrast to CIP104459, L. crispatus V4 showed high aggregation potential and 17β-estradiol promoted this phenotype. This effect was associated with large changes in cell-surface polarity and Lewis acid/base properties. In addition, we observed no effect on the membrane dynamics, contrary to CIP104459. These results can be explained by differences in the properties and organization of the S layer between the two strains. However, as for CIP104459, 17β-estradiol increased biosurfactant production of L. crispatus V4 and their adhesion to vaginal cells. This suggests that 17β-estradiol agonists would be valuable tools to favor a stable re-implantation of L. crispatus in the vaginal mucosa.