Characterization and understanding of gut microbiota has recently increased representing a wide research field, especially in autoimmune diseases. Gut microbiota is the major source of microbes which might exert beneficial as well as pathogenic effects on human health. Intestinal microbiome's role as mediator of inflammation has only recently emerged. Microbiota has been observed to differ in subjects with early rheumatoid arthritis compared to controls, and this finding has commanded this study as a possible autoimmune process. Studies with intestinal microbiota have shown that rheumatoid arthritis is characterized by an expansion and/or decrease of bacterial groups as compared to controls. In this review, we present evidence linking intestinal dysbiosis with the autoimmune mechanisms involved in the development of rheumatoid arthritis.

Obesity and overweight are health problems of multifactorial etiology, which may include changes in the microbiome. In Mexico, more than 30 % of the child population between 5 and 11 years of age suffer from being overweight or are obese, which makes it a public health issue in progress. The purpose of this work was to measure the short-chain fatty acid concentration by high-performance liquid chromatography (HPLC), and to characterize the bacterial diversity by ion torrent semiconductor sequencing, of 16S rDNA libraries prepared from stools collected from a sample of well-characterized Mexican children for normal weight, overweight, and obese conditions by anthropometric and biochemical criteria. We found that triglyceride levels are increased in overweight and obese children, who presented altered propionic and butyric acid concentrations in feces. In addition, although the colon microbiota did not show a clear bacterial dysbiosis among the three conditions, the abundance of some particular bacteria was changed with respect to normal controls. We conclude from our results that the imbalance in the abundance of at least nine different bacteria as well as altered short-chain fatty acid concentration in feces is associated to the overweight and obese conditions of Mexican children.

Obesity is a metabolic disease characterized by low-grade inflammation and accompanied by dyslipidemia and up-regulation of other bioactive molecules, creating a predisposition to endothelial dysfunction and metabolic syndrome. We studied the association between gut microbiota diversity and endothelial dysfunction (EDF) markers in obese Mexican children and adolescents. We examined clinical data including metabolic factors and EDF markers in blood samples. Gut bacterial diversity was characterized by high-throughput sequencing of V3-16S rDNA libraries. Triglycerides, insulin, homeostasis model assessment-insulin resistant (HOMA-IR), leptin, C-reactive protein (CRP), and EDF marker intercellular adhesion molecule 1 (ICAM-1) were significantly higher in obese children and adolescents. Multivariate analysis showed statistically significant positive associations between vascular cell adhesion molecule 1 (VCAM-1) and Veillonellaceae, and between ICAM-1 and Ruminococcus in obese children. In obese adolescents, there was a statistically significant positive association between total cholesterol and Ruminococcus, and between ICAM-1 and Bacteroides. LEfSe analysis showed that the genus Lactobacillus and family Coriobacteriaceae were enriched in children, and genera Collinsella and Prevotella were enriched in obese adolescents. Obese children and adolescents had higher levels of insulin resistance and metabolic syndrome. These results suggest that obese Mexican children and adolescents had increased levels of CRP and a reduction of adiponectin, which causes higher expression of EDF markers, affecting endothelial function and associating with changes in the gut microbiota.

In this work, we studied 217 Mexican subjects divided into six groups with different stages of glucose intolerance: 76 Controls (CO), 54 prediabetes (PRE), 14 T2D no medication (T2D−No−M), 14 T2D with Metformin (T2D−M), 22 T2D with polypharmacy (T2D−P), and 37 T2D with polypharmacy and insulin (T2D−P+I). We aimed to determine differences in the gut microbiota diversity for each condition. At the phylum level, we found that Firmicutes and Bacteroidetes outline major changes in the gut microbiota. The gut bacterial richness and diversity of individuals in the T2D−No−M group were lesser than other groups. Interestingly, we found a significant difference in the beta diversity of the gut microbiota among all groups. Higher abundance was found for Comamonadaceae in PRE, and Sutterella spp. in T2D−No−M. In addition, we found associations of specific microbial taxa with clinical parameters. Finally, we report predicted metabolic pathways of gut microbiota linked to T2D−M and PRE conditions. Collectively, these results indicate that each group has specific predicted metabolic characteristics and gut bacteria populations for each phenotype. The results of this study could be used to define strategies to modulate gut microbiota through noninvasive treatments, such as dietary intervention, probiotics or prebiotics, and to improve glucose tolerance of individuals with prediabetes or T2D.

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Pregnancy is a contributor to the obesity epidemic in women, probably through postpartum weight retention (PPWR), weight gain (PPWG), or a combination of both (PPWR + WG). The contribution of these patterns of postpartum weight change to long-term maternal health remains understudied. In a secondary analysis of 361 women from the prospective cohort PROGRESS, we evaluated the associations between patterns of weight change one year after delivery and cardiometabolic risk factors at six years postpartum. Using principal component analysis, we grouped cardiometabolic risk factors into: (1) body mass index (BMI), waist circumference (WC), homeostatic model assessment of insulin resistance (HOMA-IR), high-density lipoprotein cholesterol (HDL-c), triglycerides (TG), and glucose; (2) systolic (SBP) and diastolic blood pressure (DBP); and (3) low-density lipoprotein cholesterol and total cholesterol. Using path analysis, we studied direct (patterns of weight change-outcomes) and indirect associations through BMI at six years postpartum. Around 60% of women returned to their pregestational weight (reference) by one year postpartum, 6.6% experienced PPWR, 13.9% PPWG, and 19.9% PPWR + WG. Women with PPWR + WG, vs. the reference, had higher BMI and WC at six years (2.30 kg/m2, 95% CI [1.67, 2.93]; 3.38 cm [1.14, 5.62]). This was also observed in women with PPWR (1.80 kg/m2 [0.80, 2.79]; 3.15 cm [−0.35, 6.65]) and PPWG (1.22 kg/m2 [0.53, 1.92]; 3.32 cm [0.85, 5.78]). PPWR + WG had a direct association with HOMA-IR (0.21 units [0.04, 0.39]). The three patterns of weight change, vs. the reference, had significant indirect associations with HOMA-IR, glucose, TG, HDL-c, SBP, and DBP through BMI at six years. In conclusion, women with PPWR + WG are at high-risk for obesity and insulin resistance. Interventions targeting women during pregnancy and the first year postpartum may have implications for their long-term risk of obesity and cardiovascular disease.