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Inflammatory bowel diseases (IBD) result from uncontrolled inflammation in the intestinal mucosa leading to damage and loss of function. Both innate and adaptive immunity contribute to the inflammation of IBD and innate and adaptive immune cells reciprocally activate each other in a forward feedback loop. In order to better understand innate immune contributions to IBD, we developed a model of spontaneous 100% penetrant, early onset colitis that occurs in the absence of adaptive immunity by crossing villin-TNFAIP3 mice to RAG1 -/- mice (TRAG mice). This model is driven by microbes and features increased levels of innate lymphoid cells in the intestinal mucosa. To investigate the role of type 3 innate lymphoid cells (ILC3) in the innate colitis of TRAG mice, we crossed them to retinoid orphan receptor gamma t deficient (Rorγt -/- ) mice. Rorγt -/- x TRAG mice exhibited markedly reduced eosinophilia in the colonic mucosa, but colitis persisted in these mice. Colitis in Rorγt -/- x TRAG mice was characterized by increased infiltration of the intestinal mucosa by neutrophils, inflammatory monocytes, macrophages and other innate cells. RNA and cellular profiles of Rorγt -/- x TRAG mice were consistent with a lack of ILC3 and ILC3 derived cytokines, reduced antimicrobial factors, increased activation oof epithelial repair processes and reduced activation of epithelial cell STAT3. The colitis in Rorγt -/- x TRAG mice was ameliorated by antibiotic treatment indicating that microbes contribute to the ILC3-independent colitis of these mice. Together, these gene expression and cell signaling signatures reflect the double-edged sword of ILC3 in the intestine, inducing both proinflammatory and antimicrobial protective responses. Thus, Rorγt promotes eosinophilia but Rorγt and Rorγt-dependent ILC3 are dispensable for the innate colitis in TRAG mice.

The incidence of inflammatory bowel disease (IBD) is rising among racial and ethnic minorities worldwide, and studies have shown that social determinants of health impact disparities in IBD outcomes. There is a paucity of data on the impact of social determinants of health on outcomes for IBD patients transitioning from inpatient to outpatient care. The aim of our study is to quantify the linkage to care rates for IBD patients from the inpatient to the outpatient setting and to analyze the socioeconomic factors that affect linkage to care. A retrospective cohort review was conducted of all patients admitted to a tertiary academic hospital (Emory University Hospital) for a moderate to severe ulcerative colitis or Crohn’s disease flare from 01/01/2020 to 12/31/2022. We included patients who were presenting for the first time with a flare or complication of IBD, or who had not yet been linked to outpatient IBD care. We excluded patients who were already established in IBD clinic. We collected patients’ demographic information, admission data, and outpatient IBD follow-up. We linked each patient’s address to that geographic area’s deprivation index (ADI), a measure of socioeconomic disadvantage for a particular region as outlined by U. of Wisconsin Center for Health Disparities Research. Descriptive statistics and univariate/multivariate regression were performed. In our cohort of 444 patients admitted with IBD flare or complication, 30 patients met inclusion criteria. This population was 60% female/40% male. 70% had CD, 23.3% had UC, and 6.7% had indeterminate IBD. 43.3% of this group were linked to outpatient follow-up and treatment after discharge. In univariate analysis, patients who were not linked to care had a higher state and national ADI (p=0.049, 0.029). Patients not linked to care were also less likely to have an appointment scheduled at the time of hospital discharge, less likely to have MyChart/Cerner portal access and more likely to have Medicare (p=0.0003, 0.03, 0.02). Male patients were less likely to be linked to care in both univariate analysis (p=0.02) and in logistic regression, when controlling for most other study variables (p=0.01-0.03). New IBD patients living in relatively socioeconomically deprived neighborhoods were significantly less likely to be linked to care after discharge. Other social determinants of health that influenced outpatient follow-up included having private insurance and access to remote electronic medical record use. Male patients are especially vulnerable to missing IBD follow-up, even when controlling for most other variables. The most influential factor in ensuring linkage to care in this population was having a follow-up scheduled prior to discharge, emphasizing that inpatient GI teams should proactively communicate with outpatient IBD clinics to link at-risk patients to future care. Table 1: Demographics and characteristics of included IBD patients Table 2: Univariate regression of factors influencing IBD patients’ linkage to care

Inflammatory bowel diseases (IBD) result from uncontrolled inflammation in the intestinal mucosa leading to damage and loss of function. Both innate and adaptive immunity contribute to the inflammation of IBD and innate and adaptive immune cells reciprocally activate each other in a forward feedback loop. In order to better understand innate immune contributions to IBD, we developed a model of spontaneous 100% penetrant, early onset colitis that occurs in the absence of adaptive immunity by crossing villin-TNFAIP3 mice to RAG1.sup.-/- mice (TRAG mice). This model is driven by microbes and features increased levels of innate lymphoid cells in the intestinal mucosa. To investigate the role of type 3 innate lymphoid cells (ILC3) in the innate colitis of TRAG mice, we crossed them to retinoid orphan receptor gamma t deficient (Ror[gamma]t.sup.-/-) mice. Ror[gamma]t.sup.-/- x TRAG mice exhibited markedly reduced eosinophilia in the colonic mucosa, but colitis persisted in these mice. Colitis in Ror[gamma]t.sup.-/- x TRAG mice was characterized by increased infiltration of the intestinal mucosa by neutrophils, inflammatory monocytes, macrophages and other innate cells. RNA and cellular profiles of Ror[gamma]t.sup.-/- x TRAG mice were consistent with a lack of ILC3 and ILC3 derived cytokines, reduced antimicrobial factors, increased activation oof epithelial repair processes and reduced activation of epithelial cell STAT3. The colitis in Ror[gamma]t.sup.-/- x TRAG mice was ameliorated by antibiotic treatment indicating that microbes contribute to the ILC3-independent colitis of these mice. Together, these gene expression and cell signaling signatures reflect the double-edged sword of ILC3 in the intestine, inducing both proinflammatory and antimicrobial protective responses. Thus, Ror[gamma]t promotes eosinophilia but Ror[gamma]t and Ror[gamma]t-dependent ILC3 are dispensable for the innate colitis in TRAG mice.

Obesity and obesity-related metabolic disorders are linked to the intestinal microbiome. However, the causality of changes in the microbiome–host interaction affecting energy metabolism remains controversial. Here, we show the microbiome-derived metabolite δ-valerobetaine (VB) is a diet-dependent obesogen that is increased with phenotypic obesity and is correlated with visceral adipose tissue mass in humans. VB is absent in germ-free mice and their mitochondria but present in ex-germ-free conventionalized mice and their mitochondria. Mechanistic studies in vivo and in vitro show VB is produced by diverse bacterial species and inhibits mitochondrial fatty acid oxidation through decreasing cellular carnitine and mitochondrial long-chain acyl-coenzyme As. VB administration to germ-free and conventional mice increases visceral fat mass and exacerbates hepatic steatosis with a western diet but not control diet. Thus, VB provides a molecular target to understand and potentially manage microbiome–host symbiosis or dysbiosis in diet-dependent obesity. Delta-valerobetaine is a microbiome-derived metabolite that correlates with obesity-related phenotypes in humans, and exacerbates diet-induced obesity in mice.

Inflammatory bowel diseases (IBD) result from uncontrolled inflammation in the intestinal mucosa leading to damage and loss of function. Both innate and adaptive immunity contribute to the inflammation of IBD and innate and adaptive immune cells reciprocally activate each other in a forward feedback loop. In order to better understand innate immune contributions to IBD, we developed a model of spontaneous 100% penetrant, early onset colitis that occurs in the absence of adaptive immunity by crossing villin-TNFAIP3 mice to RAG1−/− mice (TRAG mice). This model is driven by microbes and features increased levels of innate lymphoid cells in the intestinal mucosa. To investigate the role of type 3 innate lymphoid cells (ILC3) in the innate colitis of TRAG mice, we crossed them to retinoid orphan receptor gamma t deficient (Rorγt−/−) mice. Rorγt−/− x TRAG mice exhibited markedly reduced eosinophilia in the colonic mucosa, but colitis persisted in these mice. Colitis in Rorγt−/− x TRAG mice was characterized by increased infiltration of the intestinal mucosa by neutrophils, inflammatory monocytes, macrophages and other innate cells. RNA and cellular profiles of Rorγt−/− x TRAG mice were consistent with a lack of ILC3 and ILC3 derived cytokines, reduced antimicrobial factors, increased activation oof epithelial repair processes and reduced activation of epithelial cell STAT3. The colitis in Rorγt−/− x TRAG mice was ameliorated by antibiotic treatment indicating that microbes contribute to the ILC3-independent colitis of these mice. Thus, Rorγt promotes eosinophilia but Rorγt and Rorγt-dependent ILC3 are dispensable for the innate colitis in TRAG mice.

The purpose of this study was to examine if the Expanded Food and Nutrition Education Program (EFNEP) pregnancy lessons have been applied by the homemakers, as reflected by differences in the dietary behavior of EFNEP homemakers as compared to non-EFNEP homemakers. The study involved the EFNEP pregnancy lessons which were part of the continuing study of the proposed 1985 impact of EFNEP nutrition education in Guam. The study sample was drawn from the EFNEP graduates and from the homemakers who had some association with, but had not participated in, the EFNEP. Thirty-seven questions were set forth for this interview. The questions included the Food Behavior Checklist, 24-Hour Food Recall, demographic characteristics, and itemized questions related to smoking and drinking during pregnancy, and food-nutrition related concerns. The questionnaire variables were analyzed and compared respondents within EFNEP groups at three time intervals: before homemakers participated in EFNEP, after homemakers participated in EFNEP, and at the time of the interview; and between groups of EFNEP and non-EFNEP homemakers. The results indicated that the Food Behavior Checklist and the 24-Hour Food Recall scores did not differ significantly between the scores of EFNEP participants, before their participation in EFNEP, and the comparison group of non-EFNEP participants. Significant differences were found between the EFNEP participant score after their participation in EFNEP and the non-EFNEP participants. The results of the data analysis for EFNEP participants before participation, after participation, and at the time of the interview showed that there was a significant difference in scores. The analysis of data for the itemized questions indicated that the homemakers' behaviors changed positively across time.