胃肠道疾病研究领域

炎症性肠病（IBD

由克罗恩病（CD）和溃疡性结肠炎（UC）组成的IBD是一种慢性炎症性疾病，在西方世界日益普遍。它被认为是由遗传易感性和环境因素的组合引起的，这些因素引发了不适当的粘膜炎症反应。IBD发病机制中微生物组的作用已经被证实与IBD患者相比，IBD患者肠道微生物组的组成和功能的改变。这与全基因组关联研究的结果是一致的，其发现许多IBD相关基因参与粘膜宿主 - 微生物相互作用，并且动物研究明在许多实验模型中在不存在微生物组的情况下对结肠炎具有抗性。

布劳恩实验室

IBD患者的微生物研究主要集中在微生物组成上。的布劳恩实验室利用multi'omic办法，包括微生物组，代表谢组，蛋白质组和分析以阐明在IBD患者的肠微生物的功能特性。微生物功能被放置在人类遗传学和疾病型/外显率的变化中。Braun博士担任CCFA微生物组织倡议的指导，并参与NIDDK IBD遗传学联盟和NIH人类微生物组项目2。

在线投稿stads产品推介着作权认知调查相关检索词肠道微生物菌落形态学肠道微生物菌落形态学肠道微生物菌落形态学肠道微生物菌落形态学细菌微生物菌落形态学能量代表谢受FUT2克罗恩病风险多态性的影响。ISME J.2014年11月; 8（11）：2193-206。doi：10.1038 / ismej.2014.64。PMID：***

McHardy IH，Goudarzi M，Tong M，Ruegger PM，Schwager E，Weger JR，Graeber TG，Sonnenburg JL，Horvath S，Huttenhower C，McGovern DP，Fornace AJ Jr，Borneman J，Braun J.微生物组和代表谢组的综合分析人的肠粘膜面展现了精妙的相互关系。微生物。2013年6月5日; 1（1）：17。doi：10.1186 / 2049-2618-1-17。PMCID***

McHardy IH，Li X，Tong M，Ruegger P，Jacobs J，Borneman J，Anton P，Braun J.HIV Infection is associated with compositional and functional shift in the rectal mucosal microbiota。

微生物。2013年10月12日; 1（1）：26。doi：10.1186 / 2049-2618-1-26。PMID：***

雅各布实验室

在雅各布实验室正在调查肠道微生物组合物的生物失活 - 即改变的组成和功能 - 是否在炎症性肠病（IBD）的发展之前。肠道微生物组和代表谢组在有高危家庭儿童IBD研究中进行了研究。在临床缓解期的IBD患者和其健康一级亲属的一个子集中观察到营养不良。这种微生物状态与影响免疫活性和上皮功能的生物活性肠代表谢物的改变有关。IBD患者的健康亲属中的生态失调的意义正在进一步探索使用人性化的gnotobiotic小鼠，以确定是否生态失调赋予增加对实验性IBD的易感性。有IBD危险的个体的痢疾可能由于遗传变异而破坏微生物的粘膜免疫系统调节。正在研究这种可能性，结合人类研究鉴定与微生物组成和敲除/转基因小鼠相关的遗传变异，以验证候选IBD相关基因和微生物组成之间的因果关系。

Jacobs JP，Braun J.Immune and genetic gardening with the intestinal microbiome。FEBS信件。588（22）：4102-11,***

Jacobs J，Braun J.宿主基因及其在肠道微生物园中的作用。基因组医学 6（12）：119，***

Jacobs等人 小儿炎症性肠病家族中的疾病相关肠型和代表谢型。消化内科。148：S-190,2015。

Pothoulakis-Koon-Rhee实验室

韩伟坤博士研究的重点是抗菌肽Cathelicidin在炎症性肠病，肠道感染，结直肠癌，肥胖和糖尿病中的合成机制和作用。Cathelicidin是一种天然的内源抗菌肽，作为先天免疫系统的一部分，对宿主有保护作用。我们的实验室首次证实内源性cathelicidin可通过骨髓来源的免疫细胞改善硫酸葡聚糖（DSS）结肠炎。我们还发现，在溃疡性结肠炎患者的结肠粘膜中单核细胞/巨噬细胞中的cathelicidin达增加。与野生型小鼠相比，Cathelicidin缺陷型小鼠发展出更严重的细菌渗入肠粘膜和相关的肠道炎症。因此，我们知道内源性cathelicidin可能是对肠道感染和炎症的保护性反应。此外，肠内施用cathelicidin肽可改善小鼠中艰难梭菌介导的结肠炎。我们正在研究cathelicidin在肥胖和糖尿病发展中肠道微生物群落变化中的作用。Koon博士现在正在研究非肽导管菌素模拟物Ceragenin CSA13在防止肠道炎症，艰难梭菌感染，肥胖和糖尿病中的作用。这种保护可能与肠道微生物群落的变化有关。CSA13比天然cathelicidin更具化学稳定性，可能适合临床使用。我们的研究利用微生物研究，临床相关的人类原代表细胞建立了一个消化疾病研究的新方向，Sang Hoon Rhee博士不仅致力于研究引起IBD的重要遗传和微生物因素，而且还致力于破译潜在的分子机制。我们最近发现在患有结肠炎症的小鼠的粪便微生物组中，酸性杆菌（Bacteroides acidifaciens）的量显着增加。相反，靶向细菌在IBD的动物模型中提供了抗炎症的保护作用。这些观察结果明酸性杆菌在结肠炎症发展和进展中的一些重要作用。因此，我们的实验室调查酸性杆菌如何调节疾病状况，以及细菌的哪些特定成分可能参与疾病的发展。

肠易激综合征和脑肠疾病

尽管神经系统和肠道之间的双向交流已经确立，但在过去的几年中，肠道菌群在这个对话中起着重要作用的临床证据才出现。在一系列高影响力的出版物中，证明了肠道微生物在调节小鼠伤害感受，情感，协会和摄取行为中的作用。一些研究还确定了与观察到的行为改变相关的大脑信号传导系统的变化。虽然大多数研究已经鉴定了无菌动物的这种行为异常，但其他人已经明，通过抗生素，益生菌和粪便移植来修饰****微生物群也可以改变行为。少数人类研究明肠道微生物，大脑功能和情绪之间可能存在关系。需要进行基础和翻译研究，以确定观察到的啮齿类动物发现在多大程度上转化为人脑肠轴（例如肠易激综合征）和人脑（包括焦虑，抑郁症，自闭症，帕金森病）的改变。

应用神经生物学Oppenheimer中心的脑微生物菌纲计划

Oppenheimer压力神经生物学中心（CNS）的脑微生物组计划旨在描述肠道微生物群及其代表谢物与健康受试者和肠易激综合征和炎症性肠病患者的结构和功能性脑标识之间的关系。这些目标是基于在啮齿动物模型中观察到的发现，以及由中心研究人员进行的初步研究证明了脑特征，肠道微生物组成和某些代表谢物之间的横截面相关性。此外，正在进行的研究旨在确定基于思维的治疗（认知行为疗法，基于正念的压力减轻）对肠道微生物组成和功能的影响。这些努力得到了NIDDK和地方试点基金的几笔赠款的支持。

Tillisch K，Labus J，Kilpatrick L，Jiang Z，Stains J，Ebrat B，Guyonnet D，Legrain-Raspaud S，Trotin B，Naliboff B，Mayer EA。用益生菌消耗发酵乳产品调节大脑活动。消化内科。2013年6月; 144（7）：1394-401,1401.e1-4。PMCID：PMC383***

Mayer EA，Tillisch K，Gupta A.肠/脑轴和微生物群。J Clin Invest。2015年3月2日; 125（3）：926-38。评论。PMCID：PMC436***

Mayer EA，Labus JS，Tillisch K，Cole SW，Baldi P.致力于IBS的系统视。Nat Rev Gastroenterol Hepatol。2015年8月25日。

Phone: (310)***

Fax: (310)***

E-mail: jbraun**[ta]**net.ucla.edu

Website: UCLA Pathology & Laboratory Medicine

医学博士 林昌

Lin Chang, MD

Director, Functional GI Disroders Program, UCLA Oppenheimer Family Center for Neurobiology of Stress; Division of Digestive Diseases, David Geffen School of Medicine at UCLA

电子邮件：linchang**[ta]**net.ucla.edu

Lin Chang, MD, is a Professor of Medicine in the Department of Medicine, Division of Digestive Diseases, at the David Geffen School of Medicine at UCLA.She serves as the Co-Director of the Center for Neurobiology of Stress at the David Geffen School of Medicine at UCLA.She is also Director of the Digestive Health and Nutrition Clinic at UCLA.Dr.Chang’s clinical expertise is in functional gastrointestinal disorders which include irritable bowel syndrome (IBS), chronic constipation, and functional dyspepsia.Dr.Chang’s research is focused on the pathophysiology of IBS related to stress, sex differences, and neuroendocrine alterations and the treatment of IBS.She is a funded NIH-investigator studying the central and peripheral mechanisms underlying IBS.

She is the recipient of the Janssen Award in Gastroenterology for Basic or Clinical Research and the AGA Distinguished Clinician Award, Dr.Chang has authored more than 70 original research articles, 48 review articles, and 19 book chapters on her specialty interests and is a frequent speaker at national and international meetings.She is a fellow of the American Gastroenterological Association and American College of Gastroenterology, and a member of the Society for Neuroscience.Dr.Chang serves as an Associate Editor of the American Journal of Gastroenterology.She is a member of the Rome Foundation Board of Directors, the Rome IV Editorial Board and the Rome IV Functional Bowel Disorders Committee.She is President of the American Neurogastroenterology and Motility Society (ANMS).She served on the FDA GI Advisory Committee from 2005-2010 which she also chaired

Omai Garner，博士

Omai Garner, PhD

Assistant Professor, Pathology & Laboratory Medicine, UCLA

A7-149 CHS

电话：（310***

电子邮件：ogarner**[ta]**net.ucla.edu

Dr.Omai Garner is a Health Sciences Assistant Clinical Professor and Associate Director of Clinical Microbiology in the UCLA Health System.He received his PhD from UC San Diego in Biomedical Sciences.He was a Postdoctoral Clinical Microbiology CPEP Fellow in the Department of Pathology at UCLA, and a former McNair Scholar.Dr.Garner is Board Certified by the American Board of Medical Microbiology.Dr.Garner’s research focuses on novel Point of Care Devices for infectious disease diagnosis in the developing world.Dr.Garner was always taught that science, at its best, is a collaborative process.”It is collaboration, and not competition, which produces the most significant advances in biomedical research.” He also serves as the Chairman of the Board for the Social Justice Learning Institute of Inglewood, California.

Cellphone-Based Hand-Held Microplate Reader for Point-of-Care Testing of Enzyme-Linked Immunosorbent Assays

Berg B, Cortazar B, Tseng D, Ozkan H, Feng S, Wei Q, Chan RY, Burbano J, Farooqui Q, Lewinski M, Di Carlo D, Garner OB, Ozcan A

ACS Nano.2015 Aug 25;9(8)***

Comparison of the Vitek MS and Bruker Microflex LT MALDI-TOF MS platforms for routine identification of commonly isolated bacteria and yeast in the clinical microbiology laboratory

Deak E, Charlton CL, Bobenchik AM, Miller SA, Pollett S, McHardy IH, Wu MT, Garner OB

Diagn Microbiol Infect Dis.2015 Jan;81(1):27

Detection of human viral pathogens: conventional versus molecular approaches

Wu MT, Garner OB

MLO Med Lab Obs.2014 Jul;46(7):8, 10-2; qui

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Arpana Gupta博士

Arpana Gupta, PhD

Adjunct Assistant Professor, Division of Digestive Diseases, David Geffen School of Medicine at UCLA; Oppenheimer Center for Neurobiology of Stress

电话：（310***

传真：（310***

电子邮件：agupta**[ta]**net.ucla.edu

网站：加州大学洛杉矶分校Oppenheimer压力神经生物学中心

Dr.Arpana (Annie) Gupta completed a PhD degree in Psychology from the University of Tennessee, Knoxville, followed by an APA accredited clinical internship at Massachusetts General Hospital/Harvard Medical Center.After coming to UCLA she joined the neuroimaging and psychophysiological cores at the Center for Neurobiology of Stress in 2012.She is currently Adjunct Assistant Professor, where she specializes in research that investigates the influence of environmental factors on shaping neurobiological phenotypes associated with stress and pain-based diseases such as obesity and functional gastroenterological disorders (FGIDs) vuvlodynia, irritable bowel syndrome.Her programmatic line of research broadly defined focuses on the bidirectional interactions between the brain and peripheral factors (in particular immune factors and gut microbiota-related metabolites) and how these interactions are modified by vulnerability (early adversity, race, adult stress, socioeconomic status SES, diet) and protective (resilience, exercise) factors in contributing to the underlying pathophysiology of these disorders.She is dedicated to using advanced automated and mathematical analytic techniques, which allows her to integrate information from multiple data sources, while accounting for sex and race differences.Her goal is to develop a comprehensive model that provides a powerful and sensitive biomarker that will increase biological readouts of these stress and pain-based disorders, thus bringing to the forefront those individuals who are at increased risk as a result of disadvantaged backgrounds.

Gupta A, Mayer EA, Sanmiguel CP, Van Horn JD, Woodworth D, Ellingson BM, Fling C, Love A, Tillisch K, Labus JS.Patterns of Brain Structural Connectivity Differentiate Lean from Overweight Subjects.Neuroimage-Clinical, 2015.13(7): 506-17.doi:10.1016/j.nicl.2015.01.005 Epub Ahead of Print.PMCID: PMC***

Mayer EA, Tillisch K, Gupta A.Gut-Brain Axis and the Microbiota.Journal of Clinical Investigation.2015; 125(3): 926-38.doi: 10.1172/JCI76304.Epub ahead of Print.PMID: 2***

Sanmiguel CP, Gupta A, Mayer EA.Gut Microbiome and Obesity: A Plausible Explanation for Obesity.Current Obesity Reports.2015.In press.

Funding Agency/Grant Number: American Psychological Fellowship – Visionary Grant

Title: “改变心灵的微生物：肥胖微生物对肥胖健康对照受试者的脑特征的影响中的性别和种族差异”

目标：拟议研究的目的是评估肥胖受试者肠道菌群对脑特征影响的性别（男性与女性）和种族（非裔美国人与非西班牙裔美国白人）之间的差异

乔纳森 雅各布博士

Phone: (310)***

E-mail: JJacobs**[ta]**net.ucla.edu

Website: Jacobs Laboratory

Dr.Jonathan Jacobs is an Assistant Professor-in-Residence in the Division of Digestive Diseases within the UCLA Department of Medicine.His research background is in immunology and the intestinal microbiome.He originally trained under Diane Mathis and Christophe Benoist at Harvard, where he published three first author papers on the immunopathological mechanisms of arthritis in an autoantibody-mediated model.He later joined Jonathan Braun’s lab at UCLA to investigate the interactions of the mucosal immune system and the intestinal microbiome in inflammatory bowel disease (IBD).He utilized human cohorts and transgenic mice to demonstrate that the IBD-associated genes RORC and TL1A, both involved in mucosal immunity, garden the intestinal microbiome.This raises the possibility that genetic risk factors promote IBD through their effects on the microbiome.An ongoing human cohort study with Dr.Braun aims to define the microbial and metabolomics features of IBD in the colonic mucosa and to characterize their relationship to IBD-associated genetic polymorphisms.In a separate translational study, he found that healthy relatives of pediatric IBD patients could be classified by their intestinal microbial and metabolomics profiles into”enterotypes” and”metabotypes” that may predict their future risk for IBD.He has authored a review article, a commentary, and two textbook chapters on intestinal host-microbiome interactions.His current research employs in vivo models and multi’omics analysis of IBD cohorts to define the role of IBD-associated genes in shaping the intestinal microbiome and to identify microbial products that promote IBD.

Jacobs JP, Lin L, Goudarzi M, Ruegger P, McGovern DPB, Fornace AJ, Borneman J, Xia L, Braun J.Microbial, metabolomic, and immunologic dynamics in a relapsing genetic mouse model of colitis induced by T-synthase deficiency.Gut Microbes.2017 Jan; 8(1):1

Jacobs JP, Goudarzi M, Singh N, Tong M, McHardy IH, Ruegger P, Asadourian M, Moon B, Ayson A, Borneman J, McGovern DPB, Fornace AJ, Braun J, Dubinsky M.A Disease-associated Enterotype and Metabotype in Healthy Relatives of Pediatric Inflammatory Bowel Disease Patients.Cellular and Molecular Gastroenterology and Hepatology.2016 Nov; 2(6)***

Jacobs JP, Braun J.Immune and genetic gardening of the intestinal microbiome.FEBS Letters.2014 Nov; 588(22):***

Complete Publications List

http://www.**bi.nlm.nih.gov/myncbi/browse/collection/4843***

Swapna Joshi博士

Swapna Joshi, PhD

Assistant Project Scientist, Center for Systems Biomedicine; Oppenheimer Center for Neurobiology of Stress; David Geffen School of Medicine at UCLA

电话：（310***

电子邮件：SwapnaJoshi**[ta]**net.ucla.edu

Dr.Swapna (Mahurkar) Joshi received her undergraduate and Master’s degree in Genetics at Osmania University, Hyderabad, India.She received her Ph.D.from Center for Cellular and Molecular Biology, Hyderabad, India.Her research interests as postdoctoral scholar at University of Southern California, Los Angeles, as well as University of California Los Angeles (UCLA) have been geared towards understanding mechanisms of various diseases including obesity, cancer and functional gastrointestinal (GI) disorders using various molecular biology and bioinformatics tools.As an assistant project scientist at UCLA, her research includes using various bioinformatics approached for integrating different data types such as, gene expression, genetic, epigenetic and microbial data to gain meaningful insights into the etiopathology of functional GI diseases including irritable bowel syndrome (IBS).Dr.Joshi has published over 23 papers in peer reviewed high impact journals

Hon Wai Koon博士

Hon Wai Koon, PhD

Assistant Professor, Division of Digestive Diseases, David Geffen School of Medicine at UCLA

电话：（310***

传真：（310***

电子邮件：hkoon**[ta]**net.ucla.edu

Dr.Koon’s research is focused on the synthetic mechanism and roles of the antimicrobial peptide Cathelicidin in inflammatory bowel disease, intestinal infections, colorectal cancer, obesity, and diabetes.Cathelicidin is a natural endogenous anti-microbial peptide that is protective to its host as a part of innate immune system.Our laboratory was the first to show that endogenous cathelicidin ameliorates dextran sulfate (DSS) colitis via bone marrow-derived immune cells.We also found increased expression of cathelicidin in monocytes/macrophages in the colonic mucosa of ulcerative colitis patients.Cathelicidin-deficient mice develop more severe bacterial penetration into intestinal mucosa and associated intestinal inflammation than wild-type mice.Therefore, we understand that endogenous cathelicidin may be a protective response to intestinal infection and inflammation.Moreover, intracolonic administration of the cathelicidin peptide ameliorates C.difficile-mediated colitis in mice.We are now studying the role of cathelicidin in the change of intestinal microflora in the development of obesity and diabetes.Dr.Koon is now investigating the role of a non-peptide cathelicidin-mimic, Ceragenin CSA13, in the protection against intestinal inflammation, C.difficile infection, obesity, and diabetes.This protection may be related to change of intestinal microflora.CSA13 is more chemically stable than natural cathelicidin and may be suitable for clinical use.Our research establishes a new direction of research in digestive diseases using microflora study, clinically relevant human primary cells, fresh intestinal biopsies, biologically induced colitis animal models, and system biology approaches.

Recent Relevant Publications

Koon HW, Shih DQ, Chen J, Bakirtzi K, Hing TC, Law I, Ho S, Ichikawa R, Zhao D, Xu H, Gallo R, Dempsey P, Cheng G, Targan SR, Pothoulakis C.Cathelicidin signaling via the Toll-like receptor protects against colitis in mice.Gastroenterology.2011 Nov;141(5):1852-63.e1-3.PubMed PMID: 21762664; PubMed Central PMCID: PMC***

Hing TC, Ho S, Shih DQ, Ichikawa R, Cheng M, Chen J, Chen X, Law I, Najarian R, Kelly CP, Gallo RL, Targan SR, Pothoulakis C, Koon HW.The antimicrobial peptide cathelicidin modulates Clostridium difficile-associated colitis and toxin A-mediated enteritis in mice.Gut.2013 Sep;62(9):1295-305.PubMed PMID: 22760006; PubMed Central PMCID: PMC***

Funding Agency/Grant Number: NIH 1R03DK103964-01A1

Title: “Role of cathelicidin in obesity and diabetes”

Jennifer Labus博士

Jennifer Labus, PhD

Director, Neuroimaging and Biostatistics Core, Oppenheimer Center for Neurobiology of Stress; Associate Professor, Division of Digestive Diseases, David Geffen School of Medicine at UCLA

电话：（310***

电子邮件：jlabus**[ta]**a.edu

Dr.Jennifer S.Labus is an Associate Professor in the David GeffenSchool of Medicine at University of California, Los Angeles.She is an investigator and Director for the Neuroimaging and Bioinformatics Core in the Oppenheimer Family Center for Neurobiology of Stress at UCLA.Her research is focused on the interface of stress, pain and emotions and its influence on the role of dysregulation in the pathophysiology of common chronic pain disorders.She has unique expertise in applying advanced statistical and computational technologies to analyze multimodal brain imaging data.She has made seminal contributions to mapping neural networks underlying visceral pain.Dr.Labus’ current research focus lies in applying a biological system based approach using bioinformatics, network analyses, supervised and unsupervised machine learning tools to integrate multimodal brain imaging data with other large scale biological data sets including genetics and metabolomics.This research provides the means to integrate and decipher large amounts of multivariate neuroimaging data to subgroup patients based on objective biological markers, and characterize central nervous system alterations for further pathophysiological investigations targeting treatment of chronic pain and obesity.She has been the recipient of a K08 Career Development award, Effective connectivity of central response in irritable bowel disorder, from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) as well as a RO3 award examining the role of altered attention and emotional arousal networks in IBS.Recently, acting as lead Co-Primary investigator she was awarded R01 funding by the National Institute of Childhood Health and Human Development (NICHD) to use brain imaging data, along with genetic, physiological and biological data, to extensively phenotype women with vulvodynia.Dr.Labus is a co-investigator on several NIH funded grants, international research collaborations, and is actively involved in mentoring graduate students and postdoctoral fellows.As a result of her work she was awarded the Master’s Award in Gastroenterology in 2010 for her outstanding achievements in Basic and Clinical Digestive Sciences.Dr.Labus was also the recipient of the American College of Neuropsychopharmacolgy Travel Award in 2

http://www.**bi.nlm.nih.gov/sites/myncbi/labusjs

Emeran Mayer，MD，PhD

Dr.Emeran Mayer is a Professor in the Departments of Medicine, Physiology and Psychiatry at the David Geffen School of Medicine at UCLA, Executive Director of the Oppenheimer Center for Neurobiology of Stress, and Co-director of the CURE: Digestive Diseases Research Center at UCLA.He is a world renowned gastroenterologist and neuroscientist with 30 years of experience in the study of clinical and neurobiological aspects of how the digestive system and the nervous system interact in health and disease, and his work has been continuously supported by the National Institutes of Health (NIH).He is currently principal investigator on 4 NIH grants including a center grant from ORWH/NIDDK on sex differences in brain gut interactions, a consortium grant by NIDDK on pelvic pain syndromes, a RO1 grant on the effects of cognitive behavioral therapy on brain signatures in IBS and a ROI grant on brain gut microbiome interactions in inflammatory and functional GI disorders (both from NIDDK).He has published over 320 peer-reviewed articles (average H index 90), including 100 chapters and reviews, co-edited four books, and organized several interdisciplinary symposia in the area of visceral pain and mind body interactions.His current research focus is on the role of the gut microbiota in modulating brain gut interactions, and their role in emotion regulation, chronic visceral pain and obesity.

Labus JS，Naliboff B，Kilpatrick L，Liu C，Ashe-McNalley C，dos Santos IR，Alaverdyan M，Woodworth D，Gupta A，Ellingson BM，Tillisch K，Mayer EA。疼痛和内窥镜成像网络（PAIN）：慢性躯体和内脏疼痛障碍的多模式，多点，大脑成像库。Neuroimage，2015 Apr 19。pii：S1053-8119（15）00308-0。doi10.1016 / j.neuroimage.2015.04.018。Epub ahead of print PMID：***

Mayer EA，Knight R，Mazmanian SK，Cryan JF，Tillisch K.Gut微生物和大脑：神经科学的范式转变。J Neurosci Nov 12; 34（46）：15490-6,2014。PMCID：PM***

Mayer EA，Labus JS，Tillisch K，Cole DE，Baldi P.，Towards a System View of Irritable Bowel Syndrome，Nat Rev Gastroenterol Hepatol。

Victoria Niklas，MD，MA

Victoria Niklas, MD, MA

Professor, Department of Pediatrics, David Geffen School of Medicine at UCLA; Director, Neonatal Intensive Care Unit and Newborn Services, Olive View-UCLA Medical Center

E-mail: niklaskrause**[ta]**a.edu

Dr.Victoria Niklas is a Professor in the Department of Pediatrics at the David Geffen School of Medicine at UCLA and the Director of the Neonatal Intensive Care Unit and Newborn Services at Olive View-UCLA Medical Center.Dr.Niklas earned her medical degree from Harvard Medical School and a master’s degree in Biochemistry and Molecular Biology from Harvard University.She completed her residency in pediatrics at Children’s Hospital Los Angeles and a fellowship in perinatal and neonatal medicine at UCLA.

Dr.Niklas has over 25 years of experience as a clinician investigator and neonatologist integrating basic and translational science in diseases afflicting the newborn.Her career has focused on understanding the immune system in the susceptibility of the newborn to infection and inflammation in the body’s largest mucosal surface, the intestine.She is a recognized expert in mouse models of intestinal immune T cell development and the pathogenesis of intestinal inflammation, in diseases such as necrotizing enterocolitis, a life-threatening intestinal disease of primarily premature infants.More recently, she was the site PI for a phase I/II RCT of enteral human recombinant lactoferrin evaluating its role in reducing hospital-acquired infections (HAI) in very low birth weight infants.Lactoferrin was safe and reduced HAI in premature infants.Also, the normally pathogenic flora was reduced in the feces of lactoferrin treated infants when compared to controls, suggesting one possible mechanism whereby lactoferrin reduced HAI in these infants.

Dr.Niklas wishes to extend these studies by exploring metagenomic signatures of maternal disease (such as obesity) in the taxonomic composition of the gut microbiota acquired by the newborn at birth.Well-described microbial signatures of obesity in adults may result in disease-associated microbial signatures in the newborn intestine.Hence, maternal flora may have a long-lasting impact on the infant’s later risk of diseases, such as obesity, in later life.The reduction in childhood obesity among breastfed infants suggests that components in breast milk (lactoferrin, milk’s microbiome, or milk oligosaccharides) may lower this risk.Possibly by influencing heritability or stability of an obesity-associated intestinal microbiome.Advanced genomic tools and sequencing will be used to explore the composition and diversity of this microbiome between mother and baby.It is, however, envisioned, that a”Mother Baby Cohort” will serve as a springboard for extended”life studies” enabling interdisciplinary, interventional and observational studies of health and disease.These endeavors will advance knowledge and ultimately improve care practices in the management in the perinatal interface with a far-reaching impact on our understanding of health and the origins of disease throughout li***

Sherman MP, Miller MM, Sherman J, Niklas V.Lactoferrin and necrotizing enterocolitis.Curr Opin Pediatr.2014 Apr; 26(2): 146-50.PubMed PMID: 2***

Sherman MP, Zaghouani H, Niklas V.Gut microbiota, the immune system, and diet influence the neonatal gut-brain axis.Pediatr Res.2015 Jan; 77(1-2): 127-35.PubMed PMID: 2***

Sherman MPS, Adamkin DH, Radmacher PG, Sherman J and Niklas V.Protective Proteins in Human Milk: Lactoferrin Steps Forward.NeoReveiws 13(5): 293-301, 2

Sherman MP, Sherman J, Arcinue R and Niklas V.Lactoferrin meets the NICU Habitat: Effects on the fecal microbiome of VLBW infants.Submitted, 2

Sherman MP，Adamkin DH，Niklas V，Radmacher P Sherman J，Wertheimer F和Petrak K.人类重组乳铁蛋白（Talactoferrin）口服液在早产儿中的随机试验，2015年准备

Charalobos Pothoulakis，MD

Charalobos Pothoulakis, MD

Director of Research, UCLA Center for Inflammatory Bowel Diseases; Professor, Pathology and Laboratory Medicine Digestive Diseases/Gastroenterology, David Geffen School of Medicine at UCLA

675 Charles E.Young Dr.South

MRL RM# 1240, Bo***

电话：（310***

电子邮件：cpothoulakis**[ta]**net.ucla.edu

Dr.Pothoulakis is the Eli and Edythe Broad Professor of Medicine at the Department of Medicine at UCLA.He is the Director of the IBD Research Center, and the Chair of Research at the Division of Digestive Diseases at UCLA..He is currently an Associate Editor for the American Journal of Physiology, Gastrointestinal and Liver Physiology and a member of the founding Editorial Board of the new AGA Journal Cellular and Molecular Gastroenterology and Hepatology.He is also the Chair of the Regulatory Peptides, Cell Signaling and Molecular Biology Section of the AGA.He is an author of over 185 original articles and numerous reviews and book chapters.His research program is primarily focused on the role of neuropeptides and hormones in several disease states, including Inflammatory Bowel Disease, Irritable Bowel Syndrome.Dr.Pothoulakis has been contributing to the Clostridium difficile field since its inception and published over 100 manuscripts in mechanisms of action of this pathogen and its toxins.He also works on mechanisms of probiotics in intestinal inflammation and he is one of the pioneers in this field.Dr.Pothoulakis’ research projects have been supported by multiple grants from the National Institutes of Health with no interruption over the past 25 years, as well as by grants from the Broad Foundation, the Crohn’s and Colitis Foundation and several pharmaceutical companies.

Kokkotou E, Moss AC, Torres D, Karagiannides I, Cheifetz A, Liu S, O’Brien M, Maratos-Flier E, Pothoulakis C.Melanin-Concentrating Hormone as a mediator of intestinal inflammation.Proc Natl Acad Sci (USA) 2008; 105:10613-8 PMCID: PM***

Savidge TC, Urvil P, Oezguen N, Kausar A, Choudhury A, Acharya V, Pinchuk I, Torres AG, English RD, Wiktorowicz JE, Leoffelholz M, Kumar R, Shi L, Nie W, Feng H, Braun W, Herman B, Stamler JS, Pothoulakis C.Host S-nitrosylation inhibits clostridial small molecule-activated glucosylating toxins.Nature Medicine; 2011; 17(9):1136-41.PMCID: PM***

Koon HW, Ho S, Hing TC, Cheng M, Chen X, Ichikawa Y, Kelly CP, Pothoulakis C.Fidaxomicin inhibits Clostridium difficile toxin A–mediated enteritis in the mouse ileum.Antimicr Agents Chemother 2014; 58(8):***

Chen X，Fruehauf J，Katchar KK，Mustafa N，Koon HW，Xu H，Zhao D，Kokkotou E，Goldsmith JD，Pothoulakis C，Kelly CP。布拉酵母（Saccharomyces boulardii）抑制Apc（min）小鼠中的EGF受体信号传导和肠肿瘤生长。胃肠病学2009; 137：91

Pothoulakis C.Review Article：布拉酵母（Saccharomyces boulardii）的抗炎作用机制。Alim Pharmacol Ther，2009; 30（8）：826-33。

Sang Hoon Rhee博士

Sang Hoon Rhee, PhD

Adjunct Associate Professor, Division of Digestive Diseases, David Geffen School of Medicine at UCLA

Dr.Rhee’s research focuses on studying roles of host-microbial interaction in the gastrointestinal tract.Specifically, the lab has been investigating the function of Toll-like receptors (TLRs) which is a family of pattern recognition receptor recognizing microbial products to elicit inflammatory and innate immune responses.Recently, Dr.Rhee demonstrated that TLR5 is associated with the development and progress of inflammatory bowel diseases.Moreover, Dr.Rhee’s studies also showed that TLR5 plays an important role to elicit innate immunity to regulate anti-tumor activity.Studies to be presented will include a role of TLR5 in regulating colon cancer and a potential mechanism to modulate anti-tumor activity against colonic tumor.This research program has a record of continuous support from the NIH/NIDDK, Crohn’s and Colitis Foundation of America, Flight Attendant Medical Research Institute at both UCLA and Harvard Medical School.

Choi YJ., Im E., Pothoulakis C., and Rhee SH.TRIF modulates TLR5-dependent responses by inducing proteolytic degradation of TLR5.(2010) The Journal of Biological Chemistry 285: 21382-21390.PMCID: PMC***

Choi YJ., Im E., Chung HK., Pothoulakis C., and Rhee SH.TRIF mediates Toll-like receptor 5-induced signaling in intestinal epithelial cells (2010) The Journal of Biological Chemistry 285:37570-37578.PMCID: PMC***

Im E., Riegler FM., Pothoulakis C., and Rhee SH. Elevated lipopolysaccharide in the colon evokes intestinal inflammation, aggravated in immune modulator-impaired mice.(2012) The American Journal of Physiology – Gastrointestinal and Liver Physiology 303(4):G490-7.PMCID: PMC3423140.(Selected as an”Editor’s Pick” from the journal)

Im E.，Jung J.和Rhee SH.，Toll样受体5啮合诱导肠上皮细胞中的IL-17C达。（2012）Journal of Interferon＆Cytokine Research 32：583-591。PMCID：PMC351***

Choi YJ，Jung J.，Chung HK，Im E.和RheeSH.，PTEN通过控制Mal / TIRAP募集来调节TLR5诱导的肠道炎症。（2013）FASEB Journal 27：243-254。PMCID：PM***

Im E.，Jung J，Pothoulakis C.，and Rhee SH.Elten speeds of pten speeds onset and increased severity of spontaneous colitis in Il10 - / - mice。（2014）胃肠病学147：667-679。PMCID：PMC4143453。