Introduction: Infectious skin diseases in athletes, particularly occur in contact sports like wrestling, football, and rugby and are caused by a variety of pathogens, including: bacteria, viruses, and fungi. These infections are common due to direct skin-to-skin contact and can lead to missed training and insufficient physical outcomes in competitions. The most frequent pathogens are methicillin-resistant Staphylococcus aureus, Trichophyton, and Herpes simplex virus. Skin infections often affect areas like the head, face, and arms and can be transmitted through contaminated equipment or direct contact. Prevention involves good hygiene, early detection, and proper disinfection of sports equipment. Effective management and isolation of infected athletes are key to reducing transmission. Purpose of the work: The aim of this review is to discuss common skin infections in contact sports, their prevalence, clinical features, diagnosis, treatment, and prevention strategies, categorized into bacterial, viral, and fungal infections. Materials and methods: A comprehensive analysis of research articles available on PubMed, Google Scholar, Web of Science, Embase, and Scopus was conducted using search terms related to: "contact sports," "skin infections," "infective skin diseases," "athletes" and "prevention." Results: Infectious skin diseases pose significant risks to athletes in contact sports due to close physical interaction, shared equipment, and skin injuries. Effective prevention requires strict hygiene, prompt wound care, and education on avoiding shared items. Awareness among coaches and athletes is crucial, as proper hygiene practices can reduce outbreaks. More research is needed to better understand transmission and to improve prevention strategies in contact sports.

Recent evidence implicates the gut microbiota in muscle physiology and function via the gut–muscle axis, which portrays bidirectional communication between microbial colonies, their metabolites and muscle tissue. Age-related muscle decline, including sarcopenia and muscle atrophy, has been associated with shifts in gut microbiota composition and lower levels of microbial metabolites, such as short-chain fatty acids (SCFAs), thereby expanding muscle health research toward microbiota-based therapies. Postbiotics, defined as preparations of inanimate microorganisms and/or their components, are gaining attention as a novel approach to combating muscle decline through modulation of microbiota–host communication, yet a comprehensive review of this topic is currently lacking. Preclinical studies demonstrate that postbiotics may exert anabolic effects while attenuating catabolism, inflammation, and cellular senescence, with associated improvements in grip strength, endurance capacity, and muscle morphology. Although clinical evidence remains limited, available studies indicate that postbiotics may have beneficial effects on muscle strength, endurance, and overall physical performance in humans. By synthesizing recent preclinical and clinical evidence, this review addresses an important gap in the literature, offering a comprehensive and mechanistically informed perspective on the potential role of postbiotics in modulating muscle health, particularly in the context of sarcopenia- and atrophy-associated muscle phenotypes.

Atopic dermatitis (AD) is a prevalent chronic inflammatory skin disorder driven by epidermal barrier defects and dysregulated Th2 cell responses. While therapies primarily address adaptive immunity, the role of Natural Killer (NK) cells remains underappreciated. This review analyzes NK cell dysfunctions in AD pathogenesis, evaluating their contributions to compromised skin immunity, microbial dysbiosis, and secondary infections. Accumulating evidence reveals a systemic deficiency of mature, cytotoxic CD56^dim and NKp80+ NK cell subsets in peripheral blood, correlating with disease severity. Within the cutaneous microenvironment, Staphylococcus aureus subverts defenses by utilizing leukocidins to lyse mature NK cells, while superantigens drive an aberrant, pro-inflammatory CD57⁻NKG2+ phenotype, exacerbating inflammation. Furthermore, localized exhaustion of functional NK cells and failure to produce interferon-gamma directly explains AD patients’ unique susceptibility to severe viral complications like eczema herpeticum. Importantly, treatments such as dupilumab and gut microbiota transplantations demonstrate that these NK cell aberrations are reversible, shifting immunity toward a normalized regulatory state. In conclusion, the NK cell compartment represents a vital regulatory axis bridging innate and adaptive immunity. Targeting this axis, particularly through IL-15 superagonists, offers a promising therapeutic frontier to suppress type 2 inflammation and restore antimicrobial defenses.