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Snow685
37 jaar vrouw, Mädchen
Ingolstadt, Germany
Marathi(Mittlere), Tamil(Grundstufe), Englisch(Fließend)
Bildhauer, Visagiste, Videographer
ID: 5218991428
Freunde: TommyLee_PL, mikeymike
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Höhe 177 cm
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Name Rose
Ansichten: 1982
Telefon: +4930929-859-55
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Beschreibung:

The main areas of research relate to the understanding of nutrition and the intestinal microbiota on gut health specifically targeting the initiation, prevention and therapy of chronic inflammatory diseases. In this context, the gut epithelium provides a primary interface for nutritional and microbial factors largely implemented in the regulation of innate and adaptive immune functions.

Mechanisms of microbe-host interactions are specified by the use of germ-free mouse models largely focusing on inflammatory bowel diseases IBD. A major focus is the identification of disease-related microbial structures relevant for the initiation and prevention of intestinal inflammation. In addition to mechanisms of microbe-host interaction, the role of cell stress related to unfolded protein responses UPR of the endoplasmic reticulum ER and mitochondria is characterized in the context of inflammatory and tumorigenic processes using novel tissue-specific mouse models.

Co-evolution of the intestinal microbiota with its host has resulted in a state of mutual benefit. Besides contributing to host nutrition, physiology and mucosal immunity, the intestinal microbiota protects the host from enteric infections, a function designated as colonization resistance. By expression of virulence and fitness factors, enteric pathogens may exploit structures and signaling pathways of the host in order to subvert specific functions of the immune system.

While host-pathogen interactions have been studied in detail during the past decades, the role of the microbiota in this interaction is largely elusive, and the trilateral interaction between enteric pathogens, the intestinal microbiota and the host is not well understood. Focus of our work is to address whether and how virulence factors of enteric pathogens, e.

Yersinia enterocolitica affect this interrelationship, and whether and how specific components of the microbiota might be used to interfere with Yersinia pathogenicity. Gnotobiotic mouse models and metagenomic analyses will provide new insights into the intricate interaction between Yersinia , the intestinal microbiota and the mucosal immune system, and might result in novel strategies for treatment of enteric infections.

Autenrieth SE, Warnke P, Wabnitz GH, Lucero Estrada C, Pasquevich KA, Drechsler D, Günter M, Hochweller K, Novakovic A, Beer-Hammer S, Samstag Y, Hämmerling GJ, Garbi N, Autenrieth IB Depletion of dendritic cells enhances innate anti-bacterial host defense through modulation of phagocyte homeostasis. PLoS Pathog Feb;8 2 :e Autenrieth SE, Linzer T-R, Hiller C, Keller B, Warnke P, Köberle M, Bohn E, Biedermann T, Bühring H-J, Hammerling GJ, Rammensee HG, Autenrieth IB Immune evasion by Yersinia enterocolitica : differential targeting of dendritic cell subpopulations in vivo.

PLoS Pathog, Nov 24;6 11 :e Köberle M, Klein-Günther A. Schütz M, Fritz M, Berchtold S, Tolosa E, Autenrieth IB, Bohn E. Yersinia enterocolitica targets cells of the innate and adaptive immune system by injection of Yops in a mouse infection model. PLoS Pathog. Aug; 5 8 :e We are interested in the evolutionary forces shaping diversity of the intestinal microbiota and its contribution to health and disease.

A combination of bacterial metagenomics, evolutionary functional genomics and population genetics is applied to identify the complex interactions between hosts, their bacteria and the environment. Front Microbiol. Int J Med Microbiol. Expression of the blood-group-related gene B4galnt2 alters susceptibility to Salmonella infection.

PLoS Pathogens, ; 11 7 :e Email: j. We seek to better understand the pathogenesis of inflammatory and infectious diseases as well as cancer of the gut. Our research specifically aims at understanding the intimate relationship between gut bacteria and the intestinal epithelium. Intestinal epithelial cells express receptors for bacterial surface molecules and are located at the frontline to the intestinal microflora.

By binding to these receptors, bacteria are able to influence the physiology of intestinal epithelial cells. As an example, gut bacteria influence survival and cell death within the intestinal epithelium, homeostatic processes that have to be strictly regulated to prevent inflammation and cancer development in the gut. Vice versa, specialized intestinal epithelial cells like Paneth cells and goblet cells express molecules, with which they control the access of gut bacteria to the epithelial surface, shape microbial communities and even kill certain bacteria.

Email: christoph. Our research focuses on the interaction of nutrition and intestinal barrier function and their impact on health maintenance and longevity. In particular, we study the role of alterations of intestinal microbiota composition and barrier function as triggers in aging-associated health decline but also in the development of liver diseases.

Using in vitro and mouse models, we aim to delineating molecular mechanisms involved in the loss of intestinal barrier function related to aging- and nutrition-associated impairments of intestinal barrier function. Herein, we especially focus on the role of dietary composition and energy bioavailability. Furthermore, diet-based prevention and therapeutic strategies to prevent alterations of intestinal barrier function and subsequently health impairments associated with these alterations are studied.

Jin CJ, Sellmann C, Engstler AJ, Ziegenhardt D, Bergheim I. Supplementation of sodium butyrate protects mice from the development of non-alcoholic steatohepatits NASH. Br J Nutr. Sellmann C, Jin CJ, Degen C, De Bandt JP, Bergheim I. Oral glutamine supplementation protects female mice from nonalcoholic steatohepatits. J Nutr. Jegatheesan P, Beutheu S, Ventura G, Nubret E, Sarfati G, Bergheim I , De Bandt JP.

Citrulline and nonessential amino acids prevent fructose-induced nonalcoholic fatty liver disease in rats. Sellmann C, Priebs J, Landmann M, Degen C, Engstler AJ, Jin CJ, Gärttner S, Spruss A, Huber O, Bergheim I. Diets rich in fructose, fat or fructose and fat alter intestinal barrier function and lead to the development of nonalcoholic fatty liver disease over time. J Nutr Biochem. Engstler AJ, Aumiller T, Degen C, Dürr M, Weiss E, Maier IB, Schattenberg JM, Jin CJ, Sellmann C, Bergheim I.

Insulin resistance alters hepatic ethanol metabolism: studies in mice and children with non-alcoholic fatty liver disease. Gut , May Our research is focused on nutrition and the gastrointestinal GI tract. For example, we aim to define molecular mechanisms how diet, food components and the intestinal microbiota affect the GI barrier at the level of mucus, enterocytes, immune cells and enteric neurons.

In turn, we want to know how the GI barrier may shape the intestinal microbiota and the intestinal mucosal immune response. Such interactions are thought to be of relevance for inflammatory e. IBD, IBS and for metabolic diseases e. Bergheim I, Weber S, Vos M, Krämer S, Volynets V, Kaserouni S, McClain CJ, Bischoff SC. Antibiotics protect against fructose-induced hepatic lipid accumulation in mice: role of endotoxin.

Journal of Hepatology ; Bischoff SC , Mailer R, Pabst O, Weier G, Sedlik W, Li Z, Chen JJ, Murphy DL, Gershon MD. Role of serotonin in intestinal inflammation: knockout of serotonin reuptake transporter exacerbates 2,4,6-trinitrobenzene sulfonic acid colitis in mice. American Journal of Physiology ; G Hagenlocher Y, Bergheim I, Zacheja S, Schäffer M, Bischoff SC , Lorentz A.

Cinnamon extract inhibits degranulation and de novo synthesis of inflammatory mediators in mast cells. Allergy ; University of Hohenheim Institute of Nutritional Medicine Dept. Stephan at uni-hohenheim. We investigate the role of the gastrointestinal microbiota in health and disease. Diet has been identified as the main factor shaping the human gut microbiome. Various nutrition-related diseases are associated with the disturbances in the gut microbiome, but the mechanisms underlying these interactions are poorly understood.

Therefore, diet-related activities of the intestinal microbiota and their consequences for the host are in the center of our research. Specific topics are:. Role of commensal bacteria in the development of inflammatory bowel disease Contribution of intestinal bacteria to the development of obesity Conversion of dietary constituents by intestinal bacteria. The overall objective is to better understand the molecular basis of host-diet-microbe interactions in the gastrointestinal tract.

We use gnotobiotic animal models and defined microbial communities to identify bacterial factors that affect regulatory and adaptive host functions. Schumann S, Alpert C, Engst W, Klopfleisch R, Loh G, Bleich A, Blaut M Mild gut inflammation modulates the proteome of intestinal Escherichia coli. Environ Microbiol Woting A, Pfeiffer N, Loh G, Klaus S, Blaut M Clostridium ramosum promotes high-fat diet-induced obesity in gnotobiotic mouse models.

MBio 5:e Budnowski J, Hanske L, Schumacher F, Glatt H, Platz S, Rohn S, Blaut, M Glucosinolates are mainly absorbed intact in germfree and human microbiota-associated mice. J Agric Food Chem Email: blaut at dife. The institute for laboratory animal science and the central animal facility of MHH Ztm , one of the largest experimental animal facilities in Europe, are closely intertwined and directed in personal union; therefore, the group aims at interrelating basic research to laboratory animal science.

Our current research interests are the pathophysiology of the gastro-intestinal mucosa particularly animal models of inflammatory bowel diseases, IBD , gnotobiology and infection models, as well as projects related to laboratory animal medicine. In the latter, we focus on murine pathogens and their effect of on animal models and sanitation methods e.

Experimental work on IBD is based on genetic quantitative trait analysis and focuses on the identification of genes and microbial factors mediating colitis susceptibility. Furthermore, the institution has a long tradition of gnotobiotic work, including generation and maintenance of germ-free models and their utilization in experimental settings.

This expertise has been successfully incorporated in various collaborations and cooperative research projects. Within the priority program, we make these techniques and experience available to the members of the SPP Buchheister, S. Bleich Nicklas, W. Keubler and A. Bleich, A. Fox

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