The skin cannot be considered as just a barrier that protects against physical, chemical, and biological damage; it is a complex and dynamic ecosystem that varies across lifespans. Interest in the relationship between physical activity and skin microbiota has grown significantly in recent years. The skin microbiota has a crucial role in skin functions and physiology, and an imbalance, known as dysbiosis, is correlated with several diseases, such as inflammatory bowel disease (IBD), infectious disease, obesity, allergic disorders, and type 1 diabetes mellitus. Among the causes of dysbiosis, the practice of physical exercise, especially in contact sports, including wrestling, artistic gymnastics, and boating, certainly represents a predisposing factor for infectious disease. This review aims to provide an overview of the skin microbiota and its regulation, focusing on interactions between physical exercise and skin microbiota, the antimicrobial peptides (AMPs) as regulators of skin microbiota, and the impact of probiotics supplementation on physical performance.

Pregnancy is characterized by significant immunological changes and a cytokine profile, as well as vitamin deficiencies that can cause problems for the correct development of a fetus. Defensins are small antimicrobial peptides that are part of the innate immune system and are involved in several biological activities. Following that, this study aims to compare the levels of various cytokines and to investigate the role of defensins between pregnant women with confirmed COVID-19 infection and pregnant women without any defined risk factor. TNF-α, TGF-β, IL-2 and IL-10, β-defensins, have been evaluated by gene expression in our population. At the same time, by ELISA assay IL-6, IL-8, defensin alpha 1, defensin beta 1 and defensin beta 4 have been measured. The data obtained show that mothers affected by COVID-19 have an increase in pro-inflammatory factors (TNF-α, TGF-β, IL-2, IL-6, IL-8) compared to controls; this increase could generate a sort of “protection of the fetus” from virus attacks. Contemporarily, we have an increase in the anti-inflammatory cytokine IL-10 and an increase in AMPs, which highlights how the mother’s body is responding to the viral attack. These results allow us to hypothesize a mechanism of “trafficking” of antimicrobial peptides from the mother to the fetus that would help the fetus to protect itself from the infection in progress.

The lack of reliable methods for preeclampsia (PE) early diagnosis limits the opportunities for timely prevention, diagnosis and treatment. This study aims to identify the alterations of biochemical parameters and the immune system activity to build a panel of markers that can support preeclampsia diagnosis. For this study, we recruited 30 pregnant women: 10 healthy pregnant women (CTR); 10 pregnant women with early preeclampsia (EP); 10 pregnant women with late preeclampsia (LP). We evaluated lipid profile and, by gene expression, we assessed PCSK9, IL-2, IL-6, IL-8, IL-10, TNF-α and TGF-β. Moreover, we evaluated both the serum and gene levels of the defensins HBD-1, HBD-2, HBD-4 and HNP-1. Our results showed an increase in gene expression levels of IL-6 and IL-8 in EP compared to LP (IL-6: median 11.7 vs 3.3, p = 0.005; IL-8: median 634.1 vs 214.1, p = 0.013) and to CTR (IL-6: median 11.7 vs 0.5, p < 0.001; IL-8: median 634.1 vs 225.6, p = 0.012), highlighting a massive activation of immune system in case of more severe preeclampsia. Furthermore, higher serum levels of HBD1 in LP compared to CTR (median: 278.8 vs 67.8, p = 0.005) and to EP (median: 278.8 vs 68.6, p = 0.001) might indicate that the same immune system puts in action protective actions to prevent adverse outcome in these cases. Finally, gene expression levels of PCSK9 decreased significantly in women with EP compared to controls and to LP (median: 0.2 vs 0.9, p = 0.010; median: 0.2 vs 1.2, p = 0.012), causing a decrease in circulating LDL-c necessary for the synthesis of placental hormones.

Intense physical activity can induce metabolic changes that modify specific biochemical biomarkers. In this scenario, the purpose of our study was to evaluate how intense physical activity can affect oxidative metabolism. Following this, fifteen professional basketball players and fifteen sedentary controls were recruited and subjected to two samplings of serum and urine in the pre-season (September) and two months after the start of the competitive season (November). Our results have shown an increase in athletes compared to controls in CK and LDH in September (respectively, p-value 0.003 and p-value < 0.001) and in November (both p-value < 0.001), whereas ALT is increased only in November (p-value 0.09). GGT serum levels were decreased in athletes compared to controls in both months (in September p-value 0.001 and in November p-value < 0.001). A gene expression analysis, carried out using RT-PCR, has revealed that IL-2, IL-6, IL-8, xCT and GCLM are increased in athletes in both months (p-value < 0.0001), while IL-10 and CHAC1 are increased only in September if compared to the controls (respectively, p-value 0.040 and p-value < 0.001). In conclusion, physical activity creates an adaptation of the systems involved in oxidative metabolism but without causing damage to the liver or kidney. This information could be of help to sports doctors for the prevention of injuries and illnesses in professional athletes for the construction of the athlete’s passport.

Background: Athletic performance is a result of interaction between genetic and environmental factors, including training, nutrition, rest, hormonal and psychophysiological status. Numerous genes and polymorphisms can influence key physiological processes, such as muscle contractility, energy metabolism, oxidative capacity, and cardiovascular efficiency. Among these, the ACTN3 gene, and in particular the polymorphism rs1815739 (NM_001104.4:c.1729C>T; p.Arg577Ter), is well known for its association with athletic performance, but emerging evidence suggests broader effects on metabolic and inflammatory phenotypes. Methods: For this study, 109 elite athletes were enrolled and genotyped for ACTN3 c.1729C>T by Sanger sequencing. Moreover, biochemical markers, such as creatine kinase (CK), C-reactive protein (CRP), lipid profile, adiponectin, and neutrophil-to-lymphocyte ratio (NLR), were examined. Finally, to better investigate the association between genotype and athletic performance, the genotypes and the results of standardized physical tests were correlated in a small exploratory subgroup of 28 professional basketball athletes. Normality was assessed using the Shapiro–Wilk test; non-normally distributed variables were summarized as median [IQR] and analyzed with non-parametric methods. Genotype comparisons were adjusted for multiple testing using the Holm procedure, and principal biochemical models were adjusted for age, BMI, sex, and ancestry. Results: The c.1729C>T genotype distribution differed between the two ancestry groups (exact p = 0.049), and all three variants were compatible with Hardy–Weinberg equilibrium within the ancestry groups. No biochemical genotype association remained statistically significant after Holm correction. In the performance subgroup, no genotype–performance association remained significant after Holm correction. Conclusions: In this cohort, the corrected analyses did not provide robust evidence for genotype-dependent biochemical or performance effects. The results are exploratory and require replication in larger cohorts, considering ancestry and gender differences.