Pseudomonas aeruginosa is a metabolically versatile opportunistic pathogen capable of surviving in a range of environments. The major contribution to these abilities relies on virulence factor production, e.g., exotoxins, phenazines, and rhamnolipids, regulated through a hierarchical system of communication, named quorum sensing (QS). QS involves the production, release, and recognition of two classes of diffusible signal molecules: N-acyl-homoserine lactones and alkyl-quinolones. These present a central role during P. aeruginosa infection, regulating bacterial virulence and the modulation of the host immune system. The influence of this arsenal of virulence factors on bacterial–host interaction makes P. aeruginosa a highly potential platform for the development of biopharmaceuticals. Here, we comprehensively reviewed the therapeutical applications of P. aeruginosa virulence factors and quorum sensing signaling molecules on pathological conditions, ranging from infections and inflammation to cancer disease.

Aquatic ecosystems have their abiotic and biotic factors constantly altered by various factors. Among them, water temperature is an abiotic factor that can significantly affect fish physiology, increasing energy demand, which can impact homeostasis and survival. Endocrine and metabolic changes and enzymatic modulation are referred to as stress responses, which can lead to oxidative stress, generating negative physiological effects when temperature limits are exceeded. Oxidative stress biomarkers used in combination can highlight the effects of a stressful condition. Here, we seek to understand how the species Astyanax lacustris , which is native to Brazil and has ecological and economic importance, as well as remarkable research potential, responds to changes in water temperature. Thus, we evaluated the effects of high (31°C ± 1°C) and low (15°C ± 1°C) thermal stress on the antioxidant defense system in the heart and kidneys of A. lacustris . Specimens were collected from artificial lakes in União da Vitória (PR) and exposed to different temperatures for periods of 2, 6, 12, 24, 48, 72, or 96 h, with a control group mantained at 23°C ± 1°C. The results indicated that in the heart exposed to 31°C, there was modulation in the biomarkers superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione (GSH), while at 15°C only GPx activity was altered. In the kidneys of fish exposed to 31°C, there was a change in the activity of the biomarkers catalase (CAT), glutathione‐S‐transferase (GST), and lipid peroxidation (LPO), while at 15°C there was modulation of the glutathione reductase (GR) biomarker and changes in the levels of reactive oxygen species (ROS). Responses to heat stress were organ‐specific, influenced by temperature and exposure time. Principal component analysis (PCA) indicated an association of glutathione‐dependent biomarkers at high temperatures in the kidneys, while responses in the heart were similar across temperatures. Overall, A. lacustris exhibited distinct antioxidant responses in different tissues under thermal stress, with kidney response being more sensitive to heat, while cardiac responses were less variable across treatments.

Frequent and excessive skin exposure to ultraviolet radiation induces oxidative stress and inflammation, raising skin diseases. Therapeutic strategies targeting both oxidative stress and inflammation may reduce skin disorders. Rhamnolipids are highly effective surface-active glycolipid biosurfactants with enormous market potential. Although these green amphiphilic molecules exhibit remarkable biomedical potential, including antimicrobial activity, wound healing properties, and analgesic effect on inflammatory pain, their therapeutic potential in UVB induced skin inflammation has not yet been investigated. A glycolipid product enriched in Dirhamnolipids (95.7%) was obtained, followed by single-step purification that provided a highly pure fraction containing 99.5% total rhamnolipids and 98.9% Dirhamnolipids (purified Di-RL). Treatment with Di-RL reduced inflammation and oxidative stress in UVB-irradiated hairless mouse skin. At a dose of 3 mg/kg, purified Di-RL reduced edema, epidermal thickening, leukocyte infiltration, myeloperoxidase activity, mast cell counts, antioxidant capacity depletion, lipid peroxidation, superoxide anion levels, and TNFα production. Collectively, these results underscore the therapeutic potential of Di-RL in the management of UVB-induced skin inflammation and oxidative stress.

Ultraviolet B (UVB) irradiation, with wavelengths ranging from 290 to 320 nm, represents a biologically active fraction of solar irradiation that reaches the Earth’s surface and exerts significant effects on human skin. Due to its high energy, UVB penetrates the epidermis and directly interacts with cellular components, particularly DNA, leading to the formation of photoproducts such as cyclobutane pyrimidine dimers. In parallel, UVB exposure induces the generation of reactive oxygen species, promoting oxidative stress and damage to lipids, proteins, and genetic material. These events activate key intracellular signaling pathways, including NF-κB and MAPKs, resulting in the production of pro-inflammatory mediators that amplify cutaneous inflammation. In addition to classical inflammatory and oxidative mechanisms, emerging evidence highlights the role of neuroimmune interactions in the skin, involving crosstalk between nerve endings, neuropeptides, and immune cells, which contributes to the regulation of local immune responses following UVB exposure. The integration of these processes plays a central role in the pathophysiology of UVB-induced skin damage and in the development of skin diseases. This review will discuss the molecular and cellular mechanisms underlying the cutaneous response triggered by UVB irradiation, with emphasis on inflammation, oxidative stress, and neuroimmune communication. Additionally, current and emerging therapeutic strategies based on pathophysiology mechanisms, including antioxidant agents, anti-inflammatory compounds, and photoprotective approaches, will be discussed to highlight potential avenues for improved prevention and treatment of UVB-induced skin damage.