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Inflammation, oxidative stress, and metabolic diseases are intricately linked in a complex, self-reinforcing relationship. Inflammation can induce oxidative stress, while oxidative stress can trigger inflammatory responses, creating a cycle that contributes to the development and progression of metabolic disorders; in addition, these effects can be observed at systemic and local scales. Both processes lead to cellular damage, mitochondrial dysfunction, and insulin resistance, particularly affecting adipose tissue, the liver, muscles, and the gastrointestinal tract. This results in impaired metabolic function and energy production, contributing to conditions such as type 2 diabetes, obesity, and metabolic syndrome. Legumes are a good source of phenolic compounds and anthocyanins that exert an antioxidant effect—they directly neutralize reactive oxygen species and free radicals, reducing oxidative stress. In vivo, in vitro, and clinical trial studies demonstrate that these compounds can modulate key cellular signaling pathways involved in inflammation and metabolism, improving insulin sensitivity and regulating lipid and glucose metabolism. They also exert anti-inflammatory effects by inhibiting proinflammatory enzymes and cytokines. Additionally, anthocyanins and phenolics may positively influence the gut microbiome, indirectly affecting metabolism and inflammation. [ABSTRACT FROM AUTHOR]

Microorganisms have a close relationship with humans, whether it is commensal, symbiotic, or pathogenic. Recently, it has been documented that microorganisms may influence the response to drug therapy. Pharmacomicrobiomics is an emerging field that focuses on the study of how variations in the microbiome affect the disposition, action, and toxicity of drugs. Two additional sciences have been added to complement pharmacomicrobiomics, namely toxicomicrobiomics, which explores how the microbiome influences drug metabolism and toxicity, and pharmacoecology, which refers to modifications in the microbiome as a result of drug administration. In this context, we introduce the concept of "drug-infection interaction" to describe the influence of pathogenic microorganisms on drug response. This review analyzes the current state of knowledge regarding the relevance of microorganisms in the host's response to drugs. It also highlights promising areas for future research and proposes the term "drug-infection interaction" as an extension of pharmacomicrobiomics. [ABSTRACT FROM AUTHOR]

Background: Macrophage migration inhibitory factor (MIF) is a cytokine capable of stimulating inflammatory cytokine and matrix metalloproteinase production from macrophages and synovial fibroblasts, which leads to persistent inflammation and bone degradation, two of the major pathological processes in rheumatoid arthritis (RA). The aim of this study was to evaluate the association of MIF promoter polymorphisms (−794CATT5‐8rs5844572 and −173G > C, rs755622), circulating MIF levels, and mRNA expression with RA susceptibility and disease activity. Methods: A case–control study was conducted in 200 RA patients and 200 control subjects (CS) from Southern Mexico. Genotyping was performed by conventional PCR and PCR‐RFLP methods. MIF mRNA expression was quantified by real‐time PCR and MIF serum levels were determined by an ELISA kit. Results: The 7,7 (−794CATT5‐8) and −173CC (−173G > C) genotypes were associated with higher disease activity in RA patients. MIF serum levels were increased, and MIF mRNA expression was reduced in RA patients as compared to CS. In addition, RA patients with moderate disease activity had higher MIF levels than those with low disease activity. The −794CATT5‐8 and −173G > C MIF polymorphisms were not associated with RA susceptibility. Conclusion: These results suggest an important role of MIF polymorphisms and MIF serum levels with disease activity in RA. [ABSTRACT FROM AUTHOR]