胃腸道疾病研究領(lǐng)域

炎癥性腸�。�IBD

由克羅恩�。�CD）和潰瘍性結(jié)腸炎（UC）組成的IBD是一種慢性炎癥性疾病，在西方世界日益普遍。它被認(rèn)為是由遺傳易感性和環(huán)境因素的組合引起的，這些因素引發(fā)了不適當(dāng)?shù)恼衬ぱ装Y反應(yīng)。IBD發(fā)病機(jī)制中微生物組的作用已經(jīng)被證實(shí)與IBD患者相比，IBD患者腸道微生物組的組成和功能的改變。這與全基因組關(guān)聯(lián)研究的結(jié)果是一致的，其發(fā)現(xiàn)許多IBD相關(guān)基因參與粘膜宿主 - 微生物相互作用，并且動(dòng)物研究明在許多實(shí)驗(yàn)?zāi)Ｐ椭性诓淮嬖谖⑸�物組的情況下對(duì)結(jié)腸炎具有抗性。

布勞恩實(shí)驗(yàn)室

IBD患者的微生物研究主要集中在微生物組成上。的布勞恩實(shí)驗(yàn)室利用multi'omic辦法，包括微生物組，代表謝組，蛋白質(zhì)組和分析以闡明在IBD患者的腸微生物的功能特性。微生物功能被放置在人類遺傳學(xué)和疾病型/外顯率的變化中。Braun博士擔(dān)任CCFA微生物組織倡議的指導(dǎo)，并參與NIDDK IBD遺傳學(xué)聯(lián)盟和NIH人類微生物組項(xiàng)目2。

在線投稿stads產(chǎn)品推介著作權(quán)認(rèn)知調(diào)查相關(guān)檢索詞腸道微生物菌落形態(tài)學(xué)腸道微生物菌落形態(tài)學(xué)腸道微生物菌落形態(tài)學(xué)腸道微生物菌落形態(tài)學(xué)細(xì)菌微生物菌落形態(tài)學(xué)能量代表謝受FUT2克羅恩病風(fēng)險(xiǎn)多態(tài)性的影響。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.微生物組和代表謝組的綜合分析人的腸粘膜面展現(xiàn)了精妙的相互關(guān)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：***

雅各布實(shí)驗(yàn)室

在雅各布實(shí)驗(yàn)室正在調(diào)查腸道微生物組合物的生物失活 - 即改變的組成和功能 - 是否在炎癥性腸�。�IBD）的發(fā)展之前。腸道微生物組和代表謝組在有高危家庭兒童IBD研究中進(jìn)行了研究。在臨床緩解期的IBD患者和其健康一級(jí)親屬的一個(gè)子集中觀察到營(yíng)養(yǎng)不良。這種微生物狀態(tài)與影響免疫活性和上皮功能的生物活性腸代表謝物的改變有關(guān)。IBD患者的健康親屬中的生態(tài)失調(diào)的意義正在進(jìn)一步探索使用人性化的gnotobiotic小鼠，以確定是否生態(tài)失調(diào)賦予增加對(duì)實(shí)驗(yàn)性IBD的易感性。有IBD危險(xiǎn)的個(gè)體的痢疾可能由于遺傳變異而破壞微生物的粘膜免疫系統(tǒng)調(diào)節(jié)。正在研究這種可能性，結(jié)合人類研究鑒定與微生物組成和敲除/轉(zhuǎn)基因小鼠相關(guān)的遺傳變異，以驗(yàn)證候選IBD相關(guān)基因和微生物組成之間的因果關(guān)系。

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

Jacobs J，Braun J.宿主基因及其在腸道微生物園中的作用�；�因組醫(yī)學(xué) 6（12）：119，***

Jacobs等人 小兒炎癥性腸病家族中的疾病相關(guān)腸型和代表謝型。消化內(nèi)科。148：S-190,2015。

Pothoulakis-Koon-Rhee實(shí)驗(yàn)室

韓偉坤博士研究的重點(diǎn)是抗菌肽Cathelicidin在炎癥性腸病，腸道感染，結(jié)直腸癌，肥胖和糖尿病中的合成機(jī)制和作用。Cathelicidin是一種天然的內(nèi)源抗菌肽，作為先天免疫系統(tǒng)的一部分，對(duì)宿主有保護(hù)作用。我們的實(shí)驗(yàn)室首次證實(shí)內(nèi)源性cathelicidin可通過(guò)骨髓來(lái)源的免疫細(xì)胞改善硫酸葡聚糖（DSS）結(jié)腸炎。我們還發(fā)現(xiàn)，在潰瘍性結(jié)腸炎患者的結(jié)腸粘膜中單核細(xì)胞/巨噬細(xì)胞中的cathelicidin達(dá)增加。與野生型小鼠相比，Cathelicidin缺陷型小鼠發(fā)展出更嚴(yán)重的細(xì)菌滲入腸粘膜和相關(guān)的腸道炎癥。因此，我們知道內(nèi)源性cathelicidin可能是對(duì)腸道感染和炎癥的保護(hù)性反應(yīng)。此外，腸內(nèi)施用cathelicidin肽可改善小鼠中艱難梭菌介導(dǎo)的結(jié)腸炎。我們正在研究cathelicidin在肥胖和糖尿病發(fā)展中腸道微生物群落變化中的作用。Koon博士現(xiàn)在正在研究非肽導(dǎo)管菌素模擬物Ceragenin CSA13在防止腸道炎癥，艱難梭菌感染，肥胖和糖尿病中的作用。這種保護(hù)可能與腸道微生物群落的變化有關(guān)。CSA13比天然cathelicidin更具化學(xué)穩(wěn)定性，可能適合臨床使用。我們的研究利用微生物研究，臨床相關(guān)的人類原代表細(xì)胞建立了一個(gè)消化疾病研究的新方向，Sang Hoon Rhee博士不僅致力于研究引起IBD的重要遺傳和微生物因素，而且還致力于破譯潛在的分子機(jī)制。我們最近發(fā)現(xiàn)在患有結(jié)腸炎癥的小鼠的糞便微生物組中，酸性桿菌（Bacteroides acidifaciens）的量顯著增加。相反，靶向細(xì)菌在IBD的動(dòng)物模型中提供了抗炎癥的保護(hù)作用。這些觀察結(jié)果明酸性桿菌在結(jié)腸炎癥發(fā)展和進(jìn)展中的一些重要作用。因此，我們的實(shí)驗(yàn)室調(diào)查酸性桿菌如何調(diào)節(jié)疾病狀況，以及細(xì)菌的哪些特定成分可能參與疾病的發(fā)展。

腸易激綜合征和腦腸疾病

盡管神經(jīng)系統(tǒng)和腸道之間的雙向交流已經(jīng)確立，但在過(guò)去的幾年中，腸道菌群在這個(gè)對(duì)話中起著重要作用的臨床證據(jù)才出現(xiàn)。在一系列高影響力的出版物中，證明了腸道微生物在調(diào)節(jié)小鼠傷害感受，情感，協(xié)會(huì)和攝取行為中的作用。一些研究還確定了與觀察到的行為改變相關(guān)的大腦信號(hào)傳導(dǎo)系統(tǒng)的變化。雖然大多數(shù)研究已經(jīng)鑒定了無(wú)菌動(dòng)物的這種行為異常，但其他人已經(jīng)明，通過(guò)抗生素，益生菌和糞便移植來(lái)修飾****微生物群也可以改變行為。少數(shù)人類研究明腸道微生物，大腦功能和情緒之間可能存在關(guān)系。需要進(jìn)行基礎(chǔ)和翻譯研究，以確定觀察到的嚙齒類動(dòng)物發(fā)現(xiàn)在多大程度上轉(zhuǎn)化為人腦腸軸（例如腸易激綜合征）和人腦（包括焦慮，抑郁癥，自閉癥，帕金森�。┑母淖儭�

應(yīng)用神經(jīng)生物學(xué)Oppenheimer中心的腦微生物菌綱計(jì)劃

Oppenheimer壓力神經(jīng)生物學(xué)中心（CNS）的腦微生物組計(jì)劃旨在描述腸道微生物群及其代表謝物與健康受試者和腸易激綜合征和炎癥性腸病患者的結(jié)構(gòu)和功能性腦標(biāo)識(shí)之間的關(guān)系。這些目標(biāo)是基于在嚙齒動(dòng)物模型中觀察到的發(fā)現(xiàn)，以及由中心研究人員進(jìn)行的初步研究證明了腦特征，腸道微生物組成和某些代表謝物之間的橫截面相關(guān)性。此外，正在進(jìn)行的研究旨在確定基于思維的治療（認(rèn)知行為療法，基于正念的壓力減輕）對(duì)腸道微生物組成和功能的影響。這些努力得到了NIDDK和地方試點(diǎn)基金的幾筆贈(zèng)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。用益生菌消耗發(fā)酵乳產(chǎn)品調(diào)節(jié)大腦活動(dòng)。消化內(nèi)科。2013年6月; 144（7）：1394-401,1401.e1-4。PMCID：PMC383***

Mayer EA，Tillisch K，Gupta A.腸/腦軸和微生物群。J Clin Invest。2015年3月2日; 125（3）：926-38。評(píng)論。PMCID：PMC436***

Mayer EA，Labus JS，Tillisch K，Cole SW，Baldi P.致力于IBS的系統(tǒng)視。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

醫(yī)學(xué)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

電子郵件：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

電話：（310***

電子郵件：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

電話：（310***

傳真：（310***

電子郵件：agupta**[ta]**net.ucla.edu

網(wǎng)站：加州大學(xué)洛杉磯分校Oppenheimer壓力神經(jīng)生物學(xué)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: “改變心靈的微生物：肥胖微生物對(duì)肥胖健康對(duì)照受試者的腦特征的影響中的性別和種族差異”

目標(biāo)：擬議研究的目的是評(píng)估肥胖受試者腸道菌群對(duì)腦特征影響的性別（男性與女性）和種族（非裔美國(guó)人與非西班牙裔美國(guó)白人）之間的差異

喬納森 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

電話：（310***

電子郵件：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

電話：（310***

傳真：（310***

電子郵件：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

電話：（310***

電子郵件：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。疼痛和內(nèi)窺鏡成像網(wǎng)絡(luò)（PAIN）：慢性軀體和內(nèi)臟疼痛障礙的多模式，多點(diǎn)，大腦成像庫(kù)。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微生物和大腦：神經(jīng)科學(xué)的范式轉(zhuǎn)變。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.人類重組乳鐵蛋白（Talactoferrin）口服液在早產(chǎn)兒中的隨機(jī)試驗(yàn)，2015年準(zhǔn)備

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***

電話：（310***

電子郵件：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受體信號(hào)傳導(dǎo)和腸腫瘤生長(zhǎng)。胃腸病學(xué)2009; 137：91

Pothoulakis C.Review Article：布拉酵母（Saccharomyces boulardii）的抗炎作用機(jī)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樣受體5嚙合誘導(dǎo)腸上皮細(xì)胞中的IL-17C達(dá)。（2012）Journal of Interferon＆Cytokine Research 32：583-591。PMCID：PMC351***

Choi YJ，Jung J.，Chung HK，Im E.和RheeSH.，PTEN通過(guò)控制Mal / TIRAP募集來(lái)調(diào)節(jié)TLR5誘導(dǎo)的腸道炎癥。（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）胃腸病學(xué)147：667-679。PMCID：PMC4143453。