Person: Sauk, Jenny S.
Loading...
Email Address
AA Acceptance Date
Birth Date
Research Projects
Organizational Units
Job Title
Last Name
Sauk
First Name
Jenny S.
Name
Sauk, Jenny S.
3 results
Search Results
Now showing 1 - 3 of 3
Publication Tethered capsule endomicroscopy enables less-invasive imaging of gastrointestinal tract microstructure(2012) Gora, Michalina J.; Sauk, Jenny S.; Carruth, Robert W.; Gallagher, Kevin A.; Suter, Melissa; Nishioka, Norman; Kava, Lauren E.; Rosenberg, Mireille; Bouma, Brett; Tearney, GuillermoHere, we introduce “tethered capsule endomicroscopy,” that involves swallowing an optomechanically-engineered pill that captures cross-sectional, 30 μm (lateral) × 7 μm (axial) resolution, microscopic images of the gut wall as it travels through the digestive tract. Results in human subjects show that this technique rapidly provides three-dimensional, microstructural images of the upper gastrointestinal tract in a simple and painless procedure, opening up new opportunities for screening for internal diseases.Publication Complex host genetics influence the microbiome in inflammatory bowel disease(BioMed Central, 2014) Knights, Dan; Silverberg, Mark S; Weersma, Rinse K; Gevers, Dirk; Dijkstra, Gerard; Huang, Hailiang; Tyler, Andrea D; van Sommeren, Suzanne; Imhann, Floris; Stempak, Joanne M; Huang, Hu; Vangay, Pajau; Al-Ghalith, Gabriel A; Russell, Caitlin; Sauk, Jenny S.; Knight, Jo; Daly, Mark; Huttenhower, Curtis; Xavier, RamnikBackground: Human genetics and host-associated microbial communities have been associated independently with a wide range of chronic diseases. One of the strongest associations in each case is inflammatory bowel disease (IBD), but disease risk cannot be explained fully by either factor individually. Recent findings point to interactions between host genetics and microbial exposures as important contributors to disease risk in IBD. These include evidence of the partial heritability of the gut microbiota and the conferral of gut mucosal inflammation by microbiome transplant even when the dysbiosis was initially genetically derived. Although there have been several tests for association of individual genetic loci with bacterial taxa, there has been no direct comparison of complex genome-microbiome associations in large cohorts of patients with an immunity-related disease. Methods: We obtained 16S ribosomal RNA (rRNA) gene sequences from intestinal biopsies as well as host genotype via Immunochip in three independent cohorts totaling 474 individuals. We tested for correlation between relative abundance of bacterial taxa and number of minor alleles at known IBD risk loci, including fine mapping of multiple risk alleles in the Nucleotide-binding oligomerization domain-containing protein 2 (NOD2) gene exon. We identified host polymorphisms whose associations with bacterial taxa were conserved across two or more cohorts, and we tested related genes for enrichment of host functional pathways. Results: We identified and confirmed in two cohorts a significant association between NOD2 risk allele count and increased relative abundance of Enterobacteriaceae, with directionality of the effect conserved in the third cohort. Forty-eight additional IBD-related SNPs have directionality of their associations with bacterial taxa significantly conserved across two or three cohorts, implicating genes enriched for regulation of innate immune response, the JAK-STAT cascade, and other immunity-related pathways. Conclusions: These results suggest complex interactions between genetically altered host functional pathways and the structure of the microbiome. Our findings demonstrate the ability to uncover novel associations from paired genome-microbiome data, and they suggest a complex link between host genetics and microbial dysbiosis in subjects with IBD across independent cohorts. Electronic supplementary material The online version of this article (doi:10.1186/s13073-014-0107-1) contains supplementary material, which is available to authorized users.Publication Early life environment and natural history of inflammatory bowel diseases(BioMed Central, 2014) Guo, Abra Y; Stevens, Betsy W; Wilson, Robin G; Russell, Caitlin N; Cohen, Melissa A; Sturgeon, Holly C; Thornton, Anna; Giallourakis, Cosmas; Khalili, Hamed; Nguyen, Deanna D; Sauk, Jenny S.; Yajnik, Vijay; Xavier, Ramnik; Ananthakrishnan, AshwinBackground: Early life exposures may modify risk of inflammatory bowel diseases (IBD; Crohn’s disease (CD), ulcerative colitis (UC)). However, the relationship between early life exposures and natural history of IBD has not been previously examined. Methods: This single center study included patients with CD or UC recruited in a prospective IBD registry. Enrolled patients completed a detailed environmental questionnaire that assessed various early life environmental exposures. Our primary outcome was requirement for disease-related surgery in CD and UC. Logistic regression models defined independent effect of early life exposures, adjusting for potential confounders. Results: Our study included 333 CD and 270 UC patients. Just over half were female with a median age at diagnosis of 25 years. One-third of the cohort had history of bowel surgery (31%) and nearly half had used at least one biologic agent (47%). Among those with CD, being breastfed was associated with reduced risk of CD-related surgery (34% vs. 55%), while childhood cigarette smoke exposure was associated with increased risk. On multivariate analysis, history of being breastfed (odds ratio (OR) 0.21, 95% confidence interval [CI] 0.09–0.46) and cigarette smoke exposure as a child (OR 2.17, 95% CI 1.10–4.29) remained independently associated with surgery. None of the early life variables influenced disease phenotype or outcome in UC. Conclusion: A history of being breastfed was associated with a decreased risk while childhood cigarette smoke exposure was associated with an increased risk of surgery in patients with CD. Further investigation to examine biological mechanisms is warranted. Electronic supplementary material The online version of this article (doi:10.1186/s12876-014-0216-8) contains supplementary material, which is available to authorized users.