Background: Microplastics (MPs) have rapidly emerged as pervasive environmental contaminants with growing implications for human health. Evidence now shows that MP exposure may begin during pregnancy and extend into infancy. Foetal exposure to MP raises questions about MP presence within reproductive organs, maternal-foetal MP transfer and the potential impact of MP on women's reproductive health. Objectives: To synthesise current evidence on the presence and distribution of microplastics in the female reproductive system and pregnancy-related organs. Methods: A systematic review of literature was conducted using Embase and Medline databases, supplemented by reference screening and manual searches. Studies were eligible if they examined MP in human female reproductive organs or pregnancy-related tissues and were published in English. Results: Eleven studies met the inclusion criteria. Across studies, MP detection varied substantially due to differences in sampling protocols, analytical techniques, and particle size detection thresholds. Cross-contamination and analytical method variability remained major methodological concerns. MP were consistently identified in follicular fluid, placental tissue, amniotic fluid, cord blood, and meconium. Conclusions: The presence of MP in both maternal and foetal compartments supports the possibility of in utero maternal-foetal MP transfer. A standardised protocol should be used to assess MP presence and MP's impact on organs and tissues. The current variability of diagnostic tests, the lack of cofounding variables control and the reduced sample sizes limit the ability to determine how clinically relevant MP exposure is during pregnancy and to women's reproductive health.

BackgroundThe role of non-nutritive sweeteners (NNS) in the development of metabolic alterations and chronic non-communicable diseases is controversial. It is also unclear whether these alterations are transmitted to offspring or whether the gut microbiota is involved in these processes. This study aimed to compare, in mice, the effect of parental sucralose or stevia consumption on fecal microbiota diversity/composition and short-chain fatty acid (SCFA) concentrations in mice, as well as on the expression of Tlr4, Tnf, Tjp1 and Srebp1 in the liver and intestines. The study also aimed to determine whether these changes are transmitted to the F1 and F2 generations.MethodsForty-seven male and female mice were divided into three groups to receive water alone or water supplemented with sucralose or stevia (0.1 mg/ml) for 16 weeks (F0 generation). The F0 mice were then bred to produce the F1 generation, and the F1 mice were bred to produce the F2 generation. The F1 and F2 animals did not receive NNS.ResultsNo changes in the glucose oral tolerance test were observed between in the F0 generation, while the glycemic response was mildly altered in the F1 and F2 male mice in the Sucralose group. Compositional changes in the fecal microbiota were greater in the F0 and F1 generations, particularly the Sucralose group. Animals from the F0 Sucralose and Stevia groups had lower SCFA concentrations, and this trait was passed on to next generations. In terms of gene expression, Tlr4 and Tnf were overexpressed in the intestine of the F0/F1 Sucralose group, while Srebp1 expression was lower in the liver of the F0 Sucralose group, a change that persisted in the F1 and F2 generations. Tlr4 and Tnf expression was higher in the F1 Stevia group and normalized in the F2.ConclusionSucralose consumption affects glucose tolerance, the expression of liver Srebp1 and intestinal Tnf and Tlr4, fecal microbiota composition and SCFA concentrations, and these changes are transmitted across generations. The effects of stevia are mainly observed in the F1 generation.

[This corrects the article DOI: 10.3389/fmicb.2021.787554.].

El síndrome de dificultad respiratoria aguda (SDRA) es una lesión pulmonar inflamatoria caracterizada por hipoxemia de inicio agudo con infiltrados pulmonares bilaterales, que sigue asociándose a una alta morbilidad y mortalidad a pesar de los avances en la ventilación mecánica protectora. Evidencia reciente ha identificado la microbiota pulmonar como un posible factor que contribuye a la fisiopatología del SDRA. En condiciones fisiológicas, la microbiota pulmonar presenta una alta diversidad bacteriana y desempeña un papel importante en el mantenimiento de la homeostasis inmunitaria. Sin embargo, aún no se ha alcanzado un consenso sobre la muestra de referencia óptima para los estudios del microbioma. En pacientes críticos, particularmente aquellos con SDRA que requieren ventilación mecánica, un hallazgo constante es la disbiosis pulmonar, definida por una menor diversidad microbiana y una mayor abundancia de bacterias de origen intestinal. Varios factores contribuyen a este desequilibrio, incluyendo la hipoxemia, la exposición a antibióticos de amplio espectro y la naturaleza invasiva de la ventilación mecánica. La disbiosis se ha asociado con respuestas inflamatorias, tanto locales como sistémicas, y se ha propuesto como mediadora de la lesión pulmonar inducida por el ventilador. Clínicamente, se han asociado alteraciones en la microbiota pulmonar con desenlaces adversos en el SDRA, como la ventilación mecánica prolongada y el aumento de la mortalidad. Se requiere más investigación para esclarecer los mecanismos causales y evaluar si la modulación del microbioma pulmonar podría representar una diana terapéutica en el SDRA.

Ulcerative colitis (UC) and Crohn’s disease (CD), known as inflammatory bowel diseases (IBDs), result from a complex interaction of genetic, immunological, microbial and environmental factors. There is growing evidence suggesting that imbalances in the gut microbiota, or dysbiosis, play a causal role in IBD and are strongly influenced by aspects of the Western lifestyle. Diet is an important modulator of gut health, and whole cereals have attracted attention for their potential to positively shape gut microbiota and intestinal function. Germination further enhances the content of prebiotic substrates and bioactive compounds such as polyphenols, GABA and fiber, which may modulate inflammation, oxidative stress and immune responses. In vitro and clinical studies suggest that these compounds may reduce pro-inflammatory cytokines and improve symptoms in IBD, although robust evidence in patients is still lacking. Here, we provide an overview of whole and sprouted cereals and their effects on inflammation and gut microbiota, with particular focus on IBD. We also discuss the potential of sprouted grains as a complementary approach to diet alongside conventional therapy, highlighting their possible support to gut health to mitigate inflammation. Finally, we emphasize the need for further well-designed clinical studies to confirm their therapeutic potential and to better understand the mechanisms underlying their beneficial effects.

Early life gut microbiota is being increasingly recognized as a major contributor to short and/or long-term human health and diseases. However, little is known about these early-life events in the human microbiome of the lower respiratory tract. This study aims to investigate fungal and bacterial colonization in the lower airways over the first year of life by analyzing lung tissue from autopsied infants. The fungal and bacterial communities of lung tissue samples from 53 autopsied infants were characterized by Next-Generation Sequencing (NGS), based on universal PCR amplification of the ITS region and the 16S rRNA gene, respectively. Our study highlights a high degree of inter-individual variability in both fungal and bacterial communities inhabiting the infant lung. The lower respiratory tract microbiota is mainly composed of transient microorganisms that likely travel from the upper respiratory tract and do not establish permanent residence. However, it could also contain some genera identified as long-term inhabitants of the lung, which could potentially play a role in lung physiology or disease. At 3-4 months of age, important dynamic changes to the microbial community were observed, which might correspond to a transitional time period in the maturation of the lung microbiome. This timeframe represents a susceptibility period for the colonization of pathogens such as Pneumocystis. The asymptomatic colonization of Pneumocystis was associated with changes in the fungal and bacterial communities. These findings suggest that the period of 2-4 months of age is a "critical window" early in life. Pneumocystis jirovecii could be a potential pivotal ecological driver contributing to shifts in microbial equilibrium during the early-life lower airway microbiome assembly, and to the future health of children.

Overweight/obesity (OW/OB) has been associated with gut dysbiosis, changes in gastrointestinal motility and sedentary behavior, contributing to metabolic and inflammatory alterations. This systematic review aims to assess the evidence supporting the influence of physical activity and exercise on gut microbiota composition and diversity in OW/OB and was conducted according to Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, using MEDLINE, EMBASE, EBSCO, and Scopus databases. Risk of bias was assessed with RoB 2 for randomized controlled trials (RCTs), ROBINS-I for non-RCT, and JBI Critical Appraisal tool for cross-sectional studies. Eleven studies were selected including 476 OW/OB and 382 normal weight individuals. Seven studies included different types of exercise intervention while the other four were cross-sectional studies assessing physical activity. Results show no clear evidence of a less diverse microbiota in OW/OB. Exercise does not significantly affect alpha diversity of gut microbiota but modifies beta diversity depending on OB status. Moderate to vigorous physical activity positively associates with gut microbiota composition and short-chain fatty acid producing bacteria. These findings highlight the importance of considering gut microbiota contribution to inter-individual variability of response to obesity treatments. Modulation of gut microbiota through physical activity should be considered in the design of personalized therapeutic strategies in obesity. PROSPERO registration number: CRD42021262107.

Metabolic dysfunction-associated steatotic liver disease (MASLD) has become highly prevalent worldwide, and its pathogenesis and progression mechanisms remain incompletely understood. An increased activation of innate immune cells in the liver contributes to hepatic fibrogenesis via a chronic loop of inflammation and regeneration processes. Among them are mast cells (MCs), whose role in hepatic cirrhosis secondary to MASLD remains poorly studied. Our aim was to evaluate differences in MC density in cirrhotic liver tissue among patients with MASLD and other chronic liver disease etiologies. For this, a retrospective study of MC count was performed in cirrhotic liver explants obtained from MASLD, alcohol-related liver disease (ALD), and autoimmune hepatitis (AIH). We included a control group of subjects without liver damage. Tryptase-positive MCs were identified by indirect immunofluorescence and quantified as MC density per low-power field (MC/LPF). Group differences were analyzed using the Kruskal-Wallis test with Dunn's multiple comparisons, considering p < 0.05 as statistically significant. A significantly higher MC density was observed in MASLD, ALD, and AIH patients compared with the control group. The group analysis showed that ALD patients exhibited higher MC density than AIH, with no observed difference between ALD and MASLD. MC density was correlated positively with tobacco smoking and alcohol use in the full analyzed group, suggesting them as risk factors of high MC liver infiltration. We conclude that MC density is augmented in MASLD-related cirrhosis, highlighting potential links between lifestyle factors and MC-mediated hepatic inflammation. Future studies should explore the mechanisms driving this association and evaluate whether targeting MCs could help mitigate fibrosis progression.

PURPOSE OF REVIEW:Metabolic dysfunction-associated steatotic liver disease (MASLD) is a highly prevalent condition that can progress to fibrosis, steatohepatitis, and hepatocellular carcinoma. This review examines recent advances concerning the role of gut microbiota in MASLD and microbiota-focused interventions to positively impact disease outcome. RECENT FINDINGS:Dysbiotic microbiota and a compromised gut barrier facilitate the translocation of microbial-associated molecular patterns and harmful metabolites into the portal circulation and liver, where they exacerbate inflammatory and fibrogenic processes. Conversely, other bacterial metabolites have protective effects in the liver. Therefore, microbiota homeostasis is essential for maintaining liver health. SUMMARY:Levels of harmful bacterial metabolites including ethanol, NH 3 , trimethylamine-L-oxide, 2-oleylglycerol, and litocholic acid are often increased in patients with MASLD. Conversely, short-chain fatty acids, indole derivatives, histidine, and the acids taurodeoxycholic, 3-succinylcholic, and hyodeoxycholic are decreased. The main aim of current interventions/treatments is to reduce harmful metabolites and increase beneficial ones. These interventions include drugs (pemafibrate, metformin, obeticholic acid), natural compounds (silymarin, lupeol, dietary fiber, peptides), exogenous bacteria (probiotics, gut symbionts), special diets (Mediterranean diet, time-restricted feeding), as well as microbiota transplantation, and phage therapy. Most improve gut permeability, liver inflammation, and fibrosis through microbiota regulation, and are promising alternatives for MASLFD management. However, most results come from animal studies, while clinical trials in MASLD patients are lacking. Further research is therefore needed in this area.

Introduction: Obesity, characterised by excess adipose tissue, is a major public health problem worldwide. Brown (BAT) and beige adipose tissue participate in thermogenesis through uncoupling protein 1 (UCP1). Polyphenols including those from Calafate (a native polyphenol-rich Patagonian berry), are considered as potential anti-obesity compounds due to their pro-thermogenic characteristics. However, polyphenols are mainly metabolized by the colonic microbiota by the gut microbiota (GM) that may influence their bioactivity and bioavailability. The aim of this study was to determine the impact of dietary administration with a Calafate polyphenol-rich extract on thermogenic activity of BAT and beige adipose tissue and GM composition. Methods: 8-week-old C57BL6 mice (n=30) were divided into 4 groups to receive for 24 weeks a control diet (C), a high-fat diet alone (HF) or high-fat diet supplemented with Calafate extract (HFC) or the same high-fat diet supplemented with Calafate extract but treated with antibiotics (HFCAB) from week 19 to 20. Administration with Calafate extract (50 mg/kg. day) was carried out for 3 weeks from week 21 to 23 in the HFC and HFCAB groups. After euthanasia, gene expression of thermogenic markers was analysed in BAT and inguinal white adipose tissue (iWAT). Transmission electron microscopy was performed to assess mitochondrial morphology and cristae density in BAT. GM diversity and composition was characterized by deep sequencing with the MiSeq-Illumina platform. Results: Calafate extract administration had no effect on weight gain in mice fed a high-fat diet. However, it prevented alterations in mitochondrial cristae induced by HFD, and increased Dio2 expression in BAT and iWAT. The intervention also influenced the gut microbiota composition, preventing changes in specific bacterial taxa induced by the high-fat diet. However, the antibiotic treatment prevented in part these effects, suggesting the implications of GM. Discussion/Conclusion: These results suggest that the acute administration of a Calafate extract modulates the expression of thermogenic markers, prevents alterations in mitochondrial cristae and intestinal microbiota in preclinical models. The study highlights the complex interaction between polyphenols, thermogenesis and the gut microbiota, providing valuable insights into their potential roles in the treatment of obesity-related metabolic diseases.

The discovery that the lung harbors a diverse microbiome, as revealed by next-generation sequencing, has significantly altered our understanding of respiratory health and disease. Despite the association between the lung microbiota and disease, the nature of their relationship remains poorly understood, and culture isolation of these microorganisms could help to determine their role in lung physiology. Current procedures for processing samples from the lower respiratory tract have been shown to affect the viability of microorganisms, so it is crucial to develop new methods to improve their survival. This study aimed to improve the isolation and characterization of lung microorganisms using a bead-beating homogenization method in a mouse model. Microsphere diameter and bead-beating time affected the survival of the microorganisms (E. coli, S. aureus and C. albicans). Using 2.3 mm diameter microspheres for 60 s of bead-beating promoted the survival of both bacteria and yeast strains. After intratracheal instillation of these microorganisms in mice, approximately 70% of the cells were recovered after the tissue homogenization. To assess the efficiency of the proposed method, the diversity of bacteria was compared between the homogenate and lung tissue samples. Ninety-one genera were detected in the lung tissue, and 63 in the homogenate. Bacterial genera detected in the homogenate represented 84% of the total abundance of the microbiota identified in the lung tissue. Taken together, these results demonstrate that the tissue homogenization process developed in this study recovered the majority of the microorganisms present in the lung. This study presents a bead-beating homogenization method for effective cultivation of lung tissue microorganisms, which may help to improve the understanding of host-microbe interactions in the lung.

Background: Gut microbiota (GM) plays a crucial role in obesity pathophysiology and is heavily influenced by dietary factors. Polyphenols have shown a positive effect in preventing and treating obesity, which is blunted in the absence of GM. Pomegranate peel, known for its high content of polyphenols (ellagitannins), has been found to exhibit favorable metabolic effects in obesity. Interestingly, ellagitannins are metabolized by the action of GM. However, the specific impact of pomegranate peel extract (PPE) on GM and metabolism remains unclear. Objective: to evaluate the effect of a PPE (microencapsulated or not) on the composition of GM in high-fat diet (HFD)-fed mice and analyze its association with metabolic parameters. Methods: Male C57BL/6J mice (n = 40) were randomly distributed into five groups: control diet (CD), HFD, HFD + inulin (IN), HFD + PPE (50 mg/kg/d of total polyphenols; TP), and HFD + MPPE (50 mg/kg/d TP), for 14 weeks. Liver and serum antioxidant status were assessed. GM composition, further relative abundances, and biodiversity were calculated from cecal content samples. The bacterial community clustering was analyzed using a canonical-correlation analysis (CCA). GM parameters and metabolic outcomes were evaluated for correlation (Spearman ' s correlation), p < 0.05. Results: PPE and MPPE showed increased energy expenditure, reduced liver arachidonic acid content, elevated antioxidant capacity, and higher GM alpha diversity compared to HFD alone. Conclusion: PPE, regardless of encapsulation, ameliorated metabolic alterations induced by HFD, potentially through modulation of GM. These findings provide data on the therapeutic potential of PPE in managing obesityrelated metabolic dysfunction.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a complex disorder whose prevalence is rapidly growing in South America. The disturbances in the microbiota–gut–liver axis impact the liver damaging processes toward fibrosis. Gut microbiota status is shaped by dietary and lifestyle factors, depending on geographic location. We aimed to identify microbial signatures in a group of Chilean MASLD patients. Forty subjects were recruited, including healthy controls (HCs), overweight/obese subjects (Ow/Ob), patients with MASLD without fibrosis (MASLD/F−), and MASLD with fibrosis (MASLD/F+). Both MASLD and fibrosis were detected through elastography and/or biopsy, and fecal microbiota were analyzed through deep sequencing. Despite no differences in α- and β-diversity among all groups, a higher abundance of Bilophila and a lower presence of Defluviitaleaceae, Lachnospiraceae ND3007, and Coprobacter was found in MASLD/F− and MASLD/F+, compared to HC. Ruminococcaceae UCG-013 and Sellimonas were more abundant in MASLD/F+ than in Ow/Ob; both significantly differed between MASLD/F− and MASLD/F+, compared to HC. Significant positive correlations were observed between liver stiffness and Bifidobacterium, Prevotella, Sarcina, and Acidaminococcus abundance. Our results show that MASLD is associated with changes in bacterial taxa that are known to be involved in bile acid metabolism and SCFA production, with some of them being more specifically linked to fibrosis.

Abstract Background IBD has emerged as a worldwide disease with an increased incidence in newly industrialized countries such as Chile. This population has been underrepresented in genome-wide association studies (GWAS) because IBD genetics studies have focused mainly on North America and European populations. In addition, specific IBD risk alleles have been related to different races and ethnicities. Aim: To investigate the association of IBD risk variants reported in previous GWAS studies with clinical outcomes in our Chilean patients. Methods 192 Chilean individuals with IBD (145 UC and 47 CD) were genotyped using Illumina GSA Arrays. From IBD GWAS (Jostin et al. and Liu et al.), we selected gene variants with pGWAS value < 5x10-8 and looked for them in our Chilean IBD group. Then, we built a Chilean dataset (clinical-genotype information). Using this dataset, we performed a Spearman correlation matrix to correlate clinical outcomes with IBD variants. Further, we built regression models to predict the clinical outcomes using the variants obtained from the correlation matrix (p <0.05). Then, we selected the best models using significance testing (P values) or likelihood-based information criterion, such as the Akaike Information Criterion (AIC) and plotted the models using a Receiver Operating Characteristic Curve (ROC). Finally, to evaluate the association among variants in each model, we perform a Gene Ontology biological process enrichment analysis using PANTHER (Fisher, FDR). Results As shown in Figure 1 and Table 1, the best predictive regression models (more than 80%) for the clinical outcomes were surgery, Clinical/Endoscopy remission for more than five years, and Naïve anti-TNF. Association with genetic variants was observed significantly (p<0.05) in the enrichment analysis for the model Clinical/endoscopy remission (Table 2). Conclusion Conclusion. Candidates’ genes related to clinical outcomes in our Chilean IBD cohort were related to epithelial, innate, and adaptative immune responses and host-microbial interactions. Future research is needed to validate these findings.

Cereal β-glucans are beneficial health ingredients that reduce cholesterolemia and postprandial glycaemia. However, their impact on digestive hormones and gut microbiota is not yet fully established. Two randomized, double-blind, controlled studies were conducted. In the first study, 14 subjects ingested a breakfast with or without β-glucan from oats (5.2 g). Compared to the control, β-glucan increased orocecal transit time (p = 0.028) and decreased mean appetite score (p = 0.014) and postprandial plasma ghrelin (p = 0.030), C-peptide (p = 0.001), insulin (p = 0.06), and glucose (p = 0.0006). β-glucan increased plasma GIP (p = 0.035) and PP (p = 0.018) without affecting leptin, GLP-1, PYY, glucagon, amylin, or 7α-hydroxy-4-cholesten-3-one, a biomarker of bile acid synthesis. In the second study, 32 subjects were distributed into 2 groups to ingest daily foods with (3 g/day) or without β-glucan for 3 weeks; stools were collected before/after treatment. No changes in fecal microbiota composition/diversity (deep sequencing) were detected with β-glucans. These results indicate that acute intake of 5 g β-glucan slows transit time and decreases hunger sensation and postprandial glycaemia without affecting bile-acid synthesis, these changes being associated with decreased plasma insulin, C-peptide, and ghrelin, and increased plasma GIP and PP. However, regular daily intake of 3 g β-glucan is not sufficient to have an effect on fecal microbiota composition.

Lactose intolerance (LI) and vitamin D deficiency (VDD) have been linked to inflammatory bowel disease (IBD). We conducted an observational study in 192 Chilean IBD patients to investigate the prevalence of a specific gene variant (LCT-13910 CC genotype) associated with LI and the prevalence of VDD/Vitamin D Receptor (VDR) gene variants. Blood samples were analyzed using Illumina’s Infinium Global Screening Array. The LCT-13910 CC genotype was found in 61% of IBD patients, similar to Chilean Hispanic controls and lower than Chilean Amerindian controls. The frequency of the LCT-13910-C allele in Chilean IBD patients (0.79) was comparable to the general population and higher than Europeans (0.49). Regarding VDR and VDD variants, in our study, the rs12785878-GG variant was associated with an increased risk of IBD (OR = 2.64, CI = 1.61–4.32; p-value = 0.001). Sixty-one percent of the Chilean IBD cohort have a genetic predisposition to lactose malabsorption, and a significant proportion exhibit genetic variants associated with VDD/VDR. Screening for LI and VDD is crucial in this Latin American IBD population.

Background and aimsLatin American populations remain underrepresented in genetic studies of inflammatory bowel diseases (IBDs). Most genetic association studies of IBD rely on Caucasian, African, and Asian individuals. These associations have yet to be evaluated in detail in the Andean region of South America. We explored the contribution of IBD-reported genetic risk variants to a Chilean cohort and the ancestry contribution to IBD in this cohort.MethodsA total of 192 Chilean IBD patients were genotyped using Illumina's Global Screening Array. Genotype data were combined with similar information from 3,147 Chilean controls. The proportions of Aymara, African, European, and Mapuche ancestries were estimated using the software ADMIXTURE. We calculated the odds ratios (ORs) and 95% confidence intervals (CIs) for gender, age, and ancestry proportions. We also explored associations with previously reported IBD-risk variants independently and in conjunction with genetic ancestry.ResultsThe first and third quartiles of the proportion of Mapuche ancestry in IBD patients were 24.7 and 34.2%, respectively, and the corresponding OR was 2.30 (95%CI 1.52–3.48) for the lowest vs. the highest group. Only one variant (rs7210086) of the 180 reported IBD-risk SNPs was associated with IBD risk in the Chilean cohort (adjusted P = 0.01). This variant is related to myeloid cells.ConclusionThe type and proportion of Native American ancestry in Chileans seem to be associated with IBD risk. Variants associated with IBD risk in this Andean region were related to myeloid cells and the innate immune response.

Abstract Background Genome-wide association studies (GWAS) have identified hundreds of polymorphisms associated with an increased risk of developing IBD. Among risk genes identified by GWAS, CARD9, a gene encoding an adapter molecule involved in the innate immune response to fungi and bacteria, has been related to IBD risk. CARD9 alleles in IBD patients may have either a protective function or a high genetic risk factor such as rs4077515. Interestingly, the CARD9S12N (rs4077515) variant has a higher frequency in the Latin South American population than the Caucasian population. The relevance of rs4077515 in the risk of IBD in the Latino population is unknown. Aims (1) To estimate allele and genotype frequencies for rs4077515 in IBD patients and Chilean controls and compare with Ensembl genome database (public data available). (2) To compare the allele and genotype distributions in IBD patients and controls, including association tests and estimation of ORs according to additive, dominant and recessive penetrance models. Methods 260 IBD patients were genotyped using the TaqMan SNP genotyping technology based on qPCR. Aggregated genotype information for 3147 population-based Chilean controls was retrieved from a published study on gallstones in Chileans (Lorenzo et al., Hepatology 2021). We calculated the allele and genotype frequencies for rs4077515 and then compared these frequencies with controls. A Chi-square test of association was used under the null hypothesis of no association between genotypes and disease. Univariate and multiple logistic regression were performed (additive, dominant, and recessive penetrance models). Results Table 1 compares rs4077515 allele and genotype frequencies in Chileans and other populations (Ensembl data set). Table 2. exhibits the estimated odds ratio for IBD, CD, and UC in Chilean population. Table 3. reveals the association results for rs4077151 models in the Chilean population. Conclusion In this study, the A risk allele for rs4077515 is significantly more frequent in the Chilean population than reported in other populations such as European, but similar to Amerindian. In this Chilean cohort, the variant rs4077515 is not associated with higher IBD risk. However, this could be an effect of sample size, or patients carrying rs4077515 requires an additional factor to IBD development.