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Dive into the research topics where Marco Raith is active.

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Featured researches published by Marco Raith.


Cellular Physiology and Biochemistry | 2015

Plasma Phosphatidylcholine Alterations in Cystic Fibrosis Patients: Impaired Metabolism and Correlation with Lung Function and Inflammation

Judith Grothe; Joachim Riethmüller; Sandra M. Tschürtz; Marco Raith; Chris J. Pynn; Dieter Stoll; Wolfgang Bernhard

Background: Liver impairment, ranging from steatosis to cirrhosis, is frequent in cystic fibrosis (CF) patients and is becoming increasingly significant due to their improved life expectancy. One aspect of hepatic alterations is caused by increased fecal loss of the essential nutrient choline, following enterohepatic bile phosphatidylcholine (PC) cycle impairment. Hepatic PC synthesis, both de novo and via phosphatidylethanolamine-N-methyl-transferase (PEMT), is essential for very low-density lipoprotein (VLDL) secretion. VLDL-PC in particular contributes to the organisms supply with polyunsaturated fatty acids (LC-PUFA), namely arachidonic (C20:4) and docosahexaenoic acid (C22:6). Consequently, choline deprivation and altered hepatic PC metabolism may affect plasma PC homeostasis and extrahepatic organ function. Objectives: To investigate relationships between altered plasma choline and PC homeostasis and markers of lung function and inflammation in CF. To assess alterations in hepatic choline and PC metabolism of CF patients. Design: Quantification of plasma/serum choline and PC species in adult CF patients compared to controls. Correlation of PC with forced expiratory vital capacity (FEV1) and interleukin 6 (IL-6) concentrations. Analysis of choline and PC metabolism in CF compared to controls, using deuterated choline ([D9-methyl]-choline) labeling in vivo. Results: Mean choline and PC concentrations in CF patients were lower than in controls. Choline and PC concentrations as well as fractions of C22:6-PC and C20:4-PC correlated directly with FEV1, but inversely with IL-6. Plasma concentrations of deuterated PC were decreased for both pathways, whereas only in PC synthesized via PEMT precursor enrichment was decreased. Conclusion: In CF patients, hepatic and plasma homeostasis of choline and PC correlate with lung function and inflammation. Impaired hepatic PC metabolism, exemplarily shown in three CF patients, provides an explanation for such correlations. Larger studies are required to understand the link between hepatic PC metabolism and overall clinical performance of CF patients, and the perspective of choline substitution of these patients.


Journal of Applied Physiology | 2012

Effects of recombinant human keratinocyte growth factor on surfactant, plasma, and liver phospholipid homeostasis in hyperoxic neonatal rats.

Marco Raith; Katharina Schaal; Roland Koslowski; Heinz Fehrenbach; Christian F. Poets; Erwin Schleicher; Wolfgang Bernhard

Respiratory distress and bronchopulmonary dysplasia (BPD) are major problems in preterm infants that are often addressed by glucocorticoid treatment and increased oxygen supply, causing catabolic and injurious side effects. Recombinant human keratinocyte growth factor (rhKGF) is noncatabolic and antiapoptotic and increases surfactant pools in immature lungs. Despite its usefulness in injured neonatal lungs, the mechanisms of improved surfactant homeostasis in vivo and systemic effects on lipid homeostasis are unknown. We therefore exposed newborn rats to 85% vs. 21% oxygen and treated them systemically with rhKGF for 48 h before death at 7 days. We determined type II pneumocyte (PN-II) proliferation, surfactant protein (SP) mRNA expression, and the pulmonary metabolism of individual phosphatidylcholine (PC) species using [D(9)-methyl]choline and tandem mass spectrometry. In addition, we assessed liver and plasma lipid metabolism, addressing PC synthesis de novo, the liver-specific phosphatidylethanolamine methyl transferase (PEMT) pathway, and triglyceride concentrations. rhKGF was found to maintain PN-II proliferation and increased SP-B/C expression and surfactant PC in both normoxic and hyperoxic lungs. We found increased total PC together with decreased [D(9)-methyl]choline enrichment, suggesting decreased turnover rather than increased secretion and synthesis as the underlying mechanism. In the liver, rhKGF increased PC synthesis, both de novo and via PEMT, underlining the organotypic differences of rhKGF actions on lipid metabolism. rhKGF increased the hepatic secretion of newly synthesized polyunsaturated PC, indicating improved systemic supply with choline and essential fatty acids. We suggest that rhKGF has potential as a therapeutic agent in neonates by improving pulmonary and systemic PC homeostasis.


Journal of Applied Physiology | 2011

Increased palmitoyl-myristoyl-phosphatidylcholine in neonatal rat surfactant is lung specific and correlates with oral myristic acid supply

Wolfgang Bernhard; Marco Raith; Christopher J. Pynn; Christian Gille; Guido Stichtenoth; Dieter Stoll; Erwin Schleicher; Christian F. Poets

Surfactant predominantly comprises phosphatidylcholine (PC) species, together with phosphatidylglycerols, phosphatidylinositols, neutral lipids, and surfactant proteins-A to -D. Together, dipalmitoyl-PC (PC16:0/16:0), palmitoyl-myristoyl-PC (PC16:0/14:0), and palmitoyl-palmitoleoyl-PC (PC16:0/16:1) make up 75-80% of mammalian surfactant PC, the proportions of which vary during development and in chronic lung diseases. PC16:0/14:0, which exerts specific effects on macrophage differentiation in vitro, increases in surfactant during alveolarization (at the expense of PC16:0/16:0), a prenatal event in humans but postnatal in rats. The mechanisms responsible and the significance of this reversible increase are, however, not understood. We hypothesized that, in rats, myristic acid (C14:0) enriched milk is key to lung-specific PC16:0/14:0 increases in surfactant. We found that surfactant PC16:0/14:0 in suckling rats correlates with C14:0 concentration in plasma chylomicrons and lung tissue triglycerides, and that PC16:0/14:0 fractions reflect exogenous C14:0 supply. Significantly, C14:0 was increased neither in plasma PC, nor in liver triglycerides, free fatty acids, or PC. Lauric acid was also abundant in triglycerides, but was not incorporated into surfactant PC. Comparing a C14:0-rich milk diet with a C14:0-poor carbohydrate diet revealed increased C14:0 and decreased C16:0 in plasma and lung triglycerides, respectively. PC16:0/14:0 enrichment at the expense of PC16:0/16:0 did not impair surfactant surface tension function. However, the PC profile of the alveolar macrophages from the milk-fed animals changed from PC16:0/16:0 rich to PC16:0/14:0 rich. This was accompanied by reduced reactive oxygen species production. We propose that nutritional supply with C14:0 and its lung-specific enrichment may contribute to decreased reactive oxygen species production during alveolarization.


American Journal of Physiology-lung Cellular and Molecular Physiology | 2016

Phosphatidylcholine kinetics in neonatal rat lungs and the effects of rhuKGF and betamethasone.

Wolfgang Bernhard; Jens Gesche; Marco Raith; Christian F. Poets

Surfactant, synthesized by type II pneumocytes (PN-II), mainly comprises phosphatidylcholine (PC) and is essential to prevent neonatal respiratory distress. Furthermore, PC is essential to lung tissue growth and maintenance as a membrane component. Recent findings suggest that the lung contributes to systemic lipid homeostasis via PC export through ABC-A1 transporter expression. Hence it is important to consider pharmacological interventions in neonatal lung PC metabolism with respect to such export. Five-day-old rats were treated with carrier (control), intraperitoneal betamethasone, subcutaneous recombinant human keratinocyte growth factor (rhuKGF), or their combination for 48 h. Animals were intraperitoneally injected with 50 mg/kg [D9-methyl]choline chloride 1.5, 3.0, and 6.0 h before death at day 7, and lung lavage fluid (LLF) and tissue were harvested. Endogenous PC, D9-labeled PC species, and their water-soluble precursors (D9-)choline and (D9-)phosphocholine were determined by tandem mass spectrometry. Treatment increased secreted and tissue PC pools but did not change equilibrium composition of PC species in LLF. However, all treatments increased specific surfactant components in tissue. In control rats, peak D9-PC in lavaged lung was reached after 3 h and was decreased at 6 h. Only 13% of this net loss in lavaged lung was found in LLF. Such decrease was not present in lungs treated with betamethasone and/or with rhuKGF. D9-PC loss at 3-6 h and PC synthesis calculated from D9 enrichment of phosphocholine indicated that daily synthesis rate is higher than total pool size. We conclude that lung tissue contributes to systemic PC homeostasis in neonatal rats, which is altered by glucocorticoid and rhuKGF treatment.


Pediatric Pulmonology | 2014

Surface tension of airway aspirates withdrawn during neonatal resuscitation reflects lung maturity

Guido Stichtenoth; Gabi Walter; Romy Lange; Marco Raith; Wolfgang Bernhard; Egbert Herting

The indications for treatment of neonates with exogenous pulmonary surfactant are still discussed controversially. Some premature neonates are sufficiently treated by CPAP, others need conventional ventilation and/or surfactant. The available lung maturity tests have limitations. The captive bubble surfactometer (CBS) provides measurement of surface activity from rather small amounts of surfactant.


European Journal of Nutrition | 2014

Plasma phospholipids indicate impaired fatty acid homeostasis in preterm infants.

Wolfgang Bernhard; Marco Raith; Vera Koch; Rebecca Kunze; Christoph Maas; Harald Abele; Christian F. Poets


European Journal of Nutrition | 2015

Choline concentrations are lower in postnatal plasma of preterm infants than in cord plasma

Wolfgang Bernhard; Marco Raith; Rebecca Kunze; Vera Koch; Martin Heni; Christoph Maas; Harald Abele; Christian F. Poets


European Journal of Nutrition | 2016

Developmental changes in polyunsaturated fetal plasma phospholipids and feto-maternal plasma phospholipid ratios and their association with bronchopulmonary dysplasia

Wolfgang Bernhard; Marco Raith; Vera Koch; Christoph Maas; Harald Abele; Christian F. Poets


Archive | 2015

acid profiling of lung, brain, and serum lipids Dexamethasone treatment in the newborn rat: fatty

Eric D. Bruder; Ping C. Lee; Hershel Raff; Lauren Jacobson; Wolfgang Bernhard; Marco Raith; Katharina Schaal; Roland Koslowski; Heinz Fehrenbach; Christian F. Poets


Archive | 2015

potential regulation of the inflammatory response KGF alters gene expression in human airway epithelia

Michael J. Welsh; Lawrence S. Prince; Philip H. Karp; Thomas O. Moninger; M. Veith; T. Rausch; Bernd Müller; P. Kilb; L. S. Van Winkle; H. Fehrenbach; Vegesna Radha; Aninda Mitra; Kunal Dayma; Kotagiri Sasikumar; Wolfgang Bernhard; Marco Raith; Katharina Schaal; Roland Koslowski; Heinz Fehrenbach; Christian F. Poets

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Heinz Fehrenbach

Dresden University of Technology

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Roland Koslowski

Dresden University of Technology

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Harald Abele

University of Tübingen

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Christoph Maas

Boston Children's Hospital

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Dieter Stoll

University of Tübingen

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