The broad range of applications offered by synthetic biology and bioengineering has revolutionized the ability to design and redesign microorganisms to express specific functions, overcoming the limitations of natural biological systems. This advancement has been achieved through the use of mathematical models and genetic circuits, enabling the precise design of synthetic microbial communities. These are defined as artificially created communities through co-cultures of selected species that share similar characteristics and environments. Reprogramming an organism is carried out by inserting synthetic genetic circuits, which are designed in a controlled manner to obtain biotechnological products beneficial to humans, their health, and the environment. The potential applications in medicine, bioremediation, industry, and pharmaceuticals make the research of synthetic microbial communities a promising field for the future. However, the implementation of synthetic microbial communities carries potential risks, such as horizontal gene transfer and possible environmental impacts. It is crucial to carefully evaluate these functions and risks, considering biocontainment and the associated ethical and ecological implications.

The One Health approach offers an integrative framework to understand infectious threats, environmental factors, antimicrobial resistance (AMR) and how their interactions affect the human–animal–environment interface. This review examines the epidemiology, transmission pathways, and mechanisms of microorganisms of public health importance (bacteria, fungi, parasites, and viruses). It highlights the interconnectedness of ecosystems, where the environment plays a central role in the dissemination of pathogens, driven by climate change, globalization, agricultural intensification, and habitat degradation. AMR is a major concern, driven by the indiscriminate use of pharmaceuticals in human, veterinary, and agricultural settings, horizontal gene transfer through mobile genetic elements, and microbial evolution. The study of different pathogens is of great importance due to their high prevalence in different ecosystems, their virulence, clinical interest, and mortality rates produced. Some of them are ESKAPE bacteria, Candida auris, Plasmodium falciparum, and emerging viruses such as SARS-CoV-2, which present complex transmission dynamics influenced by ecological and health determinants. The review also addresses the effects of climate change on the persistence and geographic spread of pathogens. Successful implementation of the One Health program requires intersectoral policies, integrated surveillance systems, prudent use of antimicrobials and investment in translational science. Coordinating these strategies is essential to limit the spread of pathogens, protect biodiversity, and save global health in the face of the growing threat of infectious diseases.

Background: Psoriatic Arthritis (PsA) is a seronegative spondyloarthropathy frequently associated with psoriasis. Studies have shown different members of the KIR (Killer Immunoglobulin-like Receptor) gene family may act as potential susceptibility factors; however, data have been inconsistent or with a reduced sample size. Therefore, the objective of this investigation was to determine associations between KIR genes and PsA susceptibility a meta-analysis approach. Methods: We performed a systemic search on PubMed, Scopus, and Web of Science to identify association studies linking KIR genes with PsA susceptibility. The search cut-off was May 2019. Odds Ratio (OR), 95% Confidence Intervals (95% CI), and forest plots were obtained for each KIR gene. Publication bias was evaluated by Begg and Egger linear regression tests. Results: Five articles were included in this meta-analysis. The KIR2DL2, 2DS1, 2DS2, and 2DS3 genes were positively associated with susceptibility to PsA (OR = 1.269, p = .003; OR = 1.392, p < .001; OR = 1.279, p = .002; and OR = 1.230, p = .038, respectively). In Caucasians, positive association with susceptibility to PsA were maintained by KIR2DL2, 2DS1, and 2DS2 genes (OR = 1.257, p = .005; OR = 1.535, p = .003; and OR = 1.267, p = .004, respectively). Conclusion: These associations suggest that KIR2DL2, 2DS1, 2DS2, and 2DS3 genes are susceptibility factors for PsA.

Psoriasis (Ps) is an autoimmune dermatosis. Previous studies have shown an association between KIR genes and susceptibility to some clinical variants of Ps. Therefore, we conducted an exhaustive systematic review with meta-analysis to evaluate the relationship between KIR genes and susceptibility to clinical variants of Ps in the overall population and according to ethnicity. According to PRISMA guidelines, we performed a systematic review through PubMed and Web of Science to identify relevant available scientific publications about KIR genes and Ps. The quality of the studies was evaluated using the Newcastle-Ottawa scale. Odds ratios (OR) and 95% confidence intervals (95%CI) were estimated using random and fixed effect models for the analyzed genes. Heterogeneity was tested using Cochran's Q-Statistic and I2, and the risk of bias was tested using the Begg test and Egger linear regression. A total of 10 case-control studies were included, comprising a variable number of KIR typified genes and psoriasis vulgaris (PsV) as the main clinical variant studied. In the total pooled results, the KIR2DS1 gene (OR = 1.518, p = .010, 95%CI: 1.105 to 2.086) was related to higher susceptibility to PsV, while the KIR2DS4 (OR = 0.563, p = .005, 95%CI: 0.376 to 0.842) and KIR3DL1 (OR = 0.602, p = .040, 95%CI: 0.370 to 0.977) genes were related to protection against PsV. This meta-analysis demonstrates that subjects that carry the KIR2DS1 gene could have a potential risk factor for the development of PsV. Conversely, KIR2DS4 and 3DL1 genes appear to confer protection against PsV.