Norbert Leitinger

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Primary Appointment

Professor, Pharmacology

Education

  • PhD, University of Vienna

Research Disciplines

Biochemistry, Biophysics, Cardiovascular Biology, Experimental Pathology, Immunology, Metabolism, Molecular Biology, Molecular Pharmacology, Translational Science

Research Interests

Role of lipid oxidation products in inflammation and vascular immunology in atherosclerosis and diabetes

Research Description

Research Interests: Role of lipid oxidation products in inflammation and vascular immunology in atherosclerosis and diabetes.
1. Resolution of acute and propagation of chronic inflammation.
2. Mechanisms of endothelial-monocyte interaction in chronic inflammation.
3. Intracellular signaling induced by oxidized lipids.
4. Pattern recognition in innate immunity (Toll like receptors).
5. Antiinflammatory activities of PPARs.
6. Regulation of heme oxygenase-1.
Techniques in Use: Quantitative RT-PCR, Promoter-reporter assays, Gel shift, siRNA, Transfection, HPLC and ESI-MS, TLC, Cell culture, Immunohistochemistry, Flow cytometry, SDS-PAGE, Western blotting, Mouse models of inflammation.
Current Summary:
Inflammation is generally accompanied by tissue damage associated with oxidation of host macromolecules by inflammation-derived free radicals. Recent evidence suggests that phospholipid oxidation products (OxPL), which are generated by oxidation of cellular membranes, lipoproteins and during apoptosis, represent danger signals that modulate inflammation and the activation of the innate immune response. My laboratory has recently demonstrated that certain OxPL are potent negative feedback regulators of innate immune responses via blocking the interaction of endotoxin with its Toll-like receptor-4 (TLR-4). Ongoing projects aim to 1) identify mechanisms by which OxPL modulate a specific immune response and delineate pathways that determine the signal differentiation between OxPL (altered self) and pathogen-associated molecular patterns (PAMPs) such as LPS (non-self), 2) investigate how acute inflammation is resolved or driven into a chronic state by OxPL, and 3) examine how monocyte specificity is brought about in chronic inflammation. The long-term goals of this research are to understand how oxidative modification of lipids during tissue damage leads to an inadequate immune response during infection, causes disruption of the tightly controlled balance of immune tolerance, and ultimately provokes chronic inflammation.
Peroxisomal proliferator activated receptors (PPARs) are ligand-activated transcription factors belonging to the superfamily of nuclear hormone receptors. In addition to regulating the fatty acid and glucose metabolism in liver, myocardium and adipose tissue, they have been shown to exert direct anti-inflammatory effects in the vascular wall, although the underlying mechanisms are poorly understood. Consequently PPAR ligands are able to slow down the progression of inflammatory vascular diseases like atherosclerosis and restenosis. Currently, we investigate the hypothesis that the induction of the potent anti-inflammatory gene heme oxygenase-1 (HO-1) by PPARs in the vascular wall significantly contributes to their anti-inflammatory effects.

Personal Statement

Research Interests:
Role of lipid oxidation products in inflammation and vascular immunology in atherosclerosis
and diabetes.
1. Resolution of acute and propagation of chronic inflammation.
2. Mechanisms of endothelial-monocyte interaction in chronic inflammation.
3. Intracellular signaling induced by oxidized lipids.
4. Pattern recognition in innate immunity (Toll like receptors).
5. Antiinflammatory activities of PPARs.
6. Regulation of heme oxygenase-1.
Techniques in Use:
Quantitative RT-PCR, Promoter-reporter assays, Gel shift, siRNA, Transfection,
HPLC and ESI-MS, TLC, Cell culture, Immunohistochemistry, Flow cytometry, SDS-PAGE,
Western blotting, Mouse models of inflammation.
Current Summary:
Inflammation is generally accompanied by tissue damage associated with oxidation
of host macromolecules by inflammation-derived free radicals. Recent evidence
suggests that phospholipid oxidation products (OxPL), which are generated by
oxidation of cellular membranes, lipoproteins and during apoptosis, represent
danger signals that modulate inflammation and the activation of the innate immune
response. My laboratory has recently demonstrated that certain OxPL are potent
negative feedback regulators of innate immune responses via blocking the interaction
of endotoxin with its Toll-like receptor-4 (TLR-4). Ongoing projects aim to
1) identify mechanisms by which OxPL modulate a specific immune response and
delineate pathways that determine the signal differentiation between OxPL (altered
self) and pathogen-associated molecular patterns (PAMPs) such as LPS (non-self),
2) investigate how acute inflammation is resolved or driven into a chronic state
by OxPL, and 3) examine how monocyte specificity is brought about in chronic
inflammation. The long-term goals of this research are to understand how oxidative
modification of lipids during tissue damage leads to an inadequate immune response
during infection, causes disruption of the tightly controlled balance of immune
tolerance, and ultimately provokes chronic inflammation.
Peroxisomal proliferator activated receptors (PPARs) are ligand-activated transcription
factors belonging to the superfamily of nuclear hormone receptors. In addition
to regulating the fatty acid and glucose metabolism in liver, myocardium and
adipose tissue, they have been shown to exert direct anti-inflammatory effects
in the vascular wall, although the underlying mechanisms are poorly understood.
Consequently PPAR ligands are able to slow down the progression of inflammatory
vascular diseases like atherosclerosis and restenosis. Currently, we investigate
the hypothesis that the induction of the potent anti-inflammatory gene heme
oxygenase-1 (HO-1) by PPARs in the vascular wall significantly contributes to
their anti-inflammatory effects.

Training

  • Basic Cardiovascular Research Training Grant
  • Interdisciplinary Training Program in Immunology
  • Training in Cell and Molecular Biology
  • Training in the Pharmacological Sciences

Selected Publications

2024

Pavelec, C. M., Young, A. P., Luviano, H. L., Orrell, E. E., Szagdaj, A., Poudel, N., . . . Leitinger, N. (2024). Pannexin 1 Channels Control Cardiomyocyte Metabolism and Neutrophil Recruitment During Non-Ischemic Heart Failure.. bioRxiv. doi:10.1101/2023.12.29.573679

Wolpe, A. G., Luse, M. A., Baryiames, C., Schug, W. J., Wolpe, J. B., Johnstone, S. R., . . . Isakson, B. E. (2024). Pannexin-3 stabilizes the transcription factor Bcl6 in a channel-independent manner to protect against vascular oxidative stress. SCIENCE SIGNALING, 17(821). doi:10.1126/scisignal.adg2622

2022

Yeudall, S., Upchurch, C. M., Seegren, P. V., Pavelec, C. M., Greulich, J., Lemke, M. C., . . . Leitinger, N. (2022). Macrophage acetyl-CoA carboxylase regulates acute inflammation through control of glucose and lipid metabolism. SCIENCE ADVANCES, 8(47). doi:10.1126/sciadv.abq1984

Lempicki, M. D., Serbulea, V., Paul, S., Upchurch, C. M., Sahu, S., Gray, J. A., . . . Meher, A. K. (2022). BAFF 60-mer binding to BAFF receptor 3 utilizes the NF-κB1 signaling pathway to hyperactivate B cells.. FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 36 Suppl 1. doi:10.1096/fasebj.2022.36.s1.r2051

Upchurch, C. M., Yeudall, S., Pavelec, C. M., Manjegowda, M., Bochkis, I. M., Scott, M., . . . Leitinger, N. (2022). Virus-induced Hepatic Expression of an Oxidized Phospholipid-binding Antibody Fragment Prevents Initiation of Hepatic Steatosis and Progression to Fibrosis.. FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 36 Suppl 1. doi:10.1096/fasebj.2022.36.s1.l8081

Luse, M. A., Pavelic, C., Tessema, R., Cochran, J., Minshall, R. D., Leitinger, N., & Isakson, B. E. (2022). Genetic deletion of endothelial Caveolin-1 is protective against metabolic disease.. FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 36 Suppl 1. doi:10.1096/fasebj.2022.36.s1.r5416

Upchurch, C. M., Yeudall, S., Pavelec, C. M., Merk, D., Greulich, J., Manjegowda, M., . . . Leitinger, N. (2022). Targeting oxidized phospholipids by AAV-based gene therapy in mice with established hepatic steatosis prevents progression to fibrosis. SCIENCE ADVANCES, 8(28). doi:10.1126/sciadv.abn0050

Pavelce, C. M., Wolf, M., Yeudall, S., Upchurch, C., & Leitinger, N. (2022). A Critical Role for Pannexin 1 in Heart Failure Induced by Acute and Chronic Isoproterenol Administration. FASEB JOURNAL, 36. doi:10.1096/fasebj.2022.36.S1.L7728

Gilbertson, N. M., Gait, J. M., Pirtle, J. M., Kirby, J. L., Upchurch, C. M., Leitinger, N., . . . Eichner, N. Z. M. (2022). Impact of a short-term low calorie diet alone or with interval exercise on quality of life and oxidized phospholipids in obese females. PHYSIOLOGY & BEHAVIOR, 246. doi:10.1016/j.physbeh.2022.113706

2021

Spinosa, M. D., Montgomery, W. G., Lempicki, M., Srikakulapu, P., Johnsrude, M. J., McNamara, C. A., . . . Meher, A. K. (2021). B Cell-Activating Factor Antagonism Attenuates the Growth of Experimental Abdominal Aortic Aneurysm. AMERICAN JOURNAL OF PATHOLOGY, 191(12), 2231-2244. doi:10.1016/j.ajpath.2021.08.012

Goldfarb, A. N., Freeman, K. C., Sahu, R. K., Elagib, K. E., Holy, M., Arneja, A., . . . Delehanty, L. L. (2021). Iron control of erythroid microtubule cytoskeleton as a potential target in treatment of iron-restricted anemia. NATURE COMMUNICATIONS, 12(1). doi:10.1038/s41467-021-21938-2

Good, M. E., Young, A. P., Wolpe, A. G., Ma, M., Hall, P. J., Duffy, C. K., . . . Isakson, B. E. (2021). Endothelial Pannexin 1 Regulates Cardiac Response to Myocardial Infarction. CIRCULATION RESEARCH, 128(8), 1211-1213. doi:10.1161/CIRCRESAHA.120.317272

2020

Senthivinayagam, S., Serbulea, V., Upchurch, C. M., Polanowska-Grabowska, R., Mendu, S. K., Sahu, S., . . . Leitinger, N. (2021). Adaptive thermogenesis in brown adipose tissue involves activation of pannexin-1 channels. MOLECULAR METABOLISM, 44. doi:10.1016/j.molmet.2020.101130

Seegren, P. V., Downs, T. K., Stremska, M. E., Harper, L. R., Cao, R., Olson, R. J., . . . Desai, B. N. (2020). Mitochondrial Ca2+ Signaling Is an Electrometabolic Switch to Fuel Phagosome Killing. CELL REPORTS, 33(8). doi:10.1016/j.celrep.2020.108411

Martinez, B. A., Hoyle, R. G., Yeudall, S., Granade, M. E., Harris, T. E., Castle, J. D., . . . Bland, M. L. (2020). Innate immune signaling in Drosophila shifts anabolic lipid metabolism from triglyceride storage to phospholipid synthesis to support immune function. PLOS GENETICS, 16(11). doi:10.1371/journal.pgen.1009192

Kreutzberger, A. J. B., Kiessling, V., Doyle, C. A., Schenk, N., Upchurch, C. M., Elmer-Dixon, M., . . . Tamm, L. K. (2020). Distinct insulin granule subpopulations implicated in the secretory pathology of diabetes types 1 and 2. ELIFE, 9. doi:10.7554/eLife.62506

Ambati, J., Magagnoli, J., Leung, H., Wang, S. -B., Andrews, C. A., Fu, D., . . . Gelfand, B. D. (2020). Repurposing anti-inflammasome NRTIs for improving insulin sensitivity and reducing type 2 diabetes development. NATURE COMMUNICATIONS, 11(1). doi:10.1038/s41467-020-18528-z

Bories, G. F. P., Yeudall, S., Serbulea, V., Fox, T. E., Isakson, B. E., & Leitinger, N. (2020). Macrophage metabolic adaptation to heme detoxification involves CO-dependent activation of the pentose phosphate pathway. BLOOD, 136(13), 1535-1548. doi:10.1182/blood.2020004964

Kruger, N., Biwer, L. A., Good, M. E., Ruddiman, C. A., Wolpe, A. G., DeLalio, L. J., . . . Isakson, B. E. (2020). Loss of Endothelial FTO Antagonizes Obesity-Induced Metabolic and Vascular Dysfunction. CIRCULATION RESEARCH, 126(2), 232-242. doi:10.1161/CIRCRESAHA.119.315531

Cherepanova, O. A., Srikakulapu, P., Greene, E. S., Chaklader, M., Haskins, R. M., McCanna, M. E., . . . Owens, G. K. (2020). Novel Autoimmune IgM Antibody Attenuates Atherosclerosis in IgM Deficient Low-Fat Diet-Fed, but Not Western Diet-Fed Apoe-/- Mice. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 40(1), 206-219. doi:10.1161/ATVBAHA.119.312771

Yeudall, S., Leitinger, N., & Laubach, V. E. (2020). Extracellular nucleotide signaling in solid organ transplantation. AMERICAN JOURNAL OF TRANSPLANTATION, 20(3), 633-640. doi:10.1111/ajt.15651

2019

Ahern, K. W., Serbulea, V., Wingrove, C. L., Palas, Z. T., Leitinger, N., & Harris, T. E. (2019). Regioisomer-independent quantification of fatty acid oxidation products by HPLC-ESI-MS/MS analysis of sodium adducts. SCIENTIFIC REPORTS, 9. doi:10.1038/s41598-019-47693-5

2018

Morioka, S., Perry, J. S. A., Raymond, M. H., Medina, C. B., Zhu, Y., Zhao, L., . . . Ravichandran, K. S. (2018). Efferocytosis induces a novel SLC program to promote glucose uptake and lactate release. NATURE, 563(7733), 714-718. doi:10.1038/s41586-018-0735-5

Serbulea, V., Upchurch, C. M., Schappe, M. S., Voigt, P., DeWeese, D. E., Desai, B. N., . . . Leitinger, N. (2018). Macrophage phenotype and bioenergetics are controlled by oxidized phospholipids identified in lean and obese adipose tissue. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 115(27), E6254-E6263. doi:10.1073/pnas.1800544115

Adamson, S. E., Polanowska-Grabowska, R., Marqueen, K., Griffiths, R., Angdisen, J., Breevoort, S. R., . . . Leitinger, N. (2018). Deficiency of Dab2 (Disabled Homolog 2) in Myeloid Cells Exacerbates Inflammation in Liver and Atherosclerotic Plaques in LDLR (Low-Density Lipoprotein Receptor)-Null MiceBrief Report. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 38(5), 1020-1029. doi:10.1161/ATVBAHA.117.310467

Schappe, M. S., Szteyn, K., Stremska, M. E., Mendu, S. K., Downs, T. K., Seegren, P. V., . . . Desai, B. N. (2018). Chanzyme TRPM7 Mediates the Ca2+ Influx Essential for Lipopolysaccharide-Induced Toll-Like Receptor 4 Endocytosis and Macrophage Activation. IMMUNITY, 48(1), 59-+. doi:10.1016/j.immuni.2017.11.026

Kerur, N., Fukuda, S., Banerjee, D., Kim, Y., Fu, D., Apicella, I., . . . Ambati, J. (2018). cGAS drives noncanonical-inflammasome activation in age-related macular degeneration (vol 24, pg 50, 2017). NATURE MEDICINE, 24(1).

Meher, A. K., Spinosa, M., Davis, J. P., Pope, N., Laubach, V. E., Su, G., . . . Upchurch, G. R. J. (2018). Novel Role of IL (Interleukin)-1β in Neutrophil Extracellular Trap Formation and Abdominal Aortic Aneurysms. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 38(4), 843-853. doi:10.1161/ATVBAHA.117.309897

Serbulea, V., Upchurch, C. M., Ahern, K. W., Bories, G., Voigt, P., DeWeese, D. E., . . . Leitinger, N. (2018). Macrophages sensing oxidized DAMPs reprogram their metabolism to support redox homeostasis and inflammation through a TLR2-Syk-ceramide dependent mechanism. MOLECULAR METABOLISM, 7, 23-34. doi:10.1016/j.molmet.2017.11.002

2017

Good, M. E., Chiu, Y. -H., Poon, I. K. H., Medina, C. B., Butcher, J. T., Mendu, S. K., . . . Ravichandran, K. S. (2018). Pannexin 1 Channels as an Unexpected New Target of the Anti-Hypertensive Drug Spironolactone. CIRCULATION RESEARCH, 122(4), 606-615. doi:10.1161/CIRCRESAHA.117.312380

Kerur, N., Fukuda, S., Banerjee, D., Kim, Y., Fu, D., Apicella, I., . . . Ambati, J. (2018). cGAS drives noncanonical-inflammasome activation in age-related macular degeneration. NATURE MEDICINE, 24(1), 50-+. doi:10.1038/nm.4450

Adamson, S. E., Montgomery, G., Seaman, S. A., Peirce-Cottler, S. M., & Leitinger, N. (2018). Myeloid P2Y2 receptor promotes acute inflammation but is dispensable for chronic high-fat diet-induced metabolic dysfunction. PURINERGIC SIGNALLING, 14(1), 19-26. doi:10.1007/s11302-017-9589-9

Olmez, I., Brenneman, B., Xiao, A., Serbulea, V., Benamar, M., Zhang, Y., . . . Purow, B. (2017). Combined CDK4/6 and mTOR Inhibition Is Synergistic against Glioblastoma via Multiple Mechanisms. CLINICAL CANCER RESEARCH, 23(22), 6958-6968. doi:10.1158/1078-0432.CCR-17-0803

Serbulea, V., DeWeese, D., & Leitinger, N. (2017). The effect of oxidized phospholipids on phenotypic polarization and function of macrophages. FREE RADICAL BIOLOGY AND MEDICINE, 111, 156-168. doi:10.1016/j.freeradbiomed.2017.02.035

Jakobs, P., Serbulea, V., Leitinger, N., Eckers, A., & Haendeler, J. (2017). Nuclear Factor (Erythroid-Derived 2)-Like 2 and Thioredoxin-1 in Atherosclerosis and Ischemia/Reperfusion Injury in the Heart. ANTIOXIDANTS & REDOX SIGNALING, 26(12), 630-644. doi:10.1089/ars.2016.6795

Bories, G. F. P., & Leitinger, N. (2017). Macrophage metabolism in atherosclerosis. FEBS LETTERS, 591(19), 3042-3060. doi:10.1002/1873-3468.12786

Dyballa-Rukes, N., Jakobs, P., Eckers, A., Ale-Agha, N., Serbulea, V., Aufenvenne, K., . . . Haendeler, J. (2017). The Anti-Apoptotic Properties of APEX1 in the Endothelium Require the First 20 Amino Acids and Converge on Thioredoxin-1. ANTIOXIDANTS & REDOX SIGNALING, 26(12), 616-629. doi:10.1089/ars.2016.6799

2016

Wilkins, L. R., Brautigan, D. L., Wu, H., Yarmohammadi, H., Kubicka, E., Serbulea, V., . . . Haaga, J. R. (2017). Cinnamic Acid Derivatives Enhance the Efficacy of Transarterial Embolization in a Rat Model of Hepatocellular Carcinoma. CARDIOVASCULAR AND INTERVENTIONAL RADIOLOGY, 40(3), 430-437. doi:10.1007/s00270-016-1515-y

Adamson, S. E., Griffiths, R., Moravec, R., Senthivinayagam, S., Montgomery, G., Chen, W., . . . Leitinger, N. (2016). Disabled homolog 2 controls macrophage phenotypic polarization and adipose tissue inflammation. JOURNAL OF CLINICAL INVESTIGATION, 126(4), 1311-1322. doi:10.1172/JCI79590

Tosello-Trampont, A. -C., Krueger, P., Narayanan, S., Landes, S. G., Leitinger, N., & Hahn, Y. S. (2016). NKp46+ Natural Killer Cells Attenuate Metabolism-Induced Hepatic Fibrosis by Regulating Macrophage Activation in Mice. HEPATOLOGY, 63(3), 799-812. doi:10.1002/hep.28389

Schaheen, B., Downs, E. A., Serbulea, V., Almenara, C. C. P., Spinosa, M., Su, G., . . . Ailawadi, G. (2016). B-Cell Depletion Promotes Aortic Infiltration of Immunosuppressive Cells and Is Protective of Experimental Aortic Aneurysm. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 36(11), 2191-+. doi:10.1161/ATVBAHA.116.307559

2015

Adamson, S. E., Meher, A. K., Chiu, Y. -H., Sandilos, J. K., Oberholtzer, N. P., Walker, N. N., . . . Leitinger, N. (2015). Pannexin 1 is required for full activation of insulin-stimulated glucose uptake in adipocytes. MOLECULAR METABOLISM, 4(9), 610-618. doi:10.1016/j.molmet.2015.06.009

Rothe, T., Gruber, F., Uderhardt, S., Ipseiz, N., Roessner, S., Oskolkova, O., . . . Kroenke, G. (2015). 12/15-lipoxygenase-mediated enzymatic lipid oxidation regulates DC maturation and function. JOURNAL OF CLINICAL INVESTIGATION, 125(5), 1944-1954. doi:10.1172/JCI78490

Lohman, A. W., Leskov, I. L., Butcher, J. T., Johnstone, S. R., Stokes, T. A., Begandt, D., . . . Isakson, B. E. (2015). Pannexin 1 channels regulate leukocyte emigration through the venous endothelium during acute inflammation. NATURE COMMUNICATIONS, 6. doi:10.1038/ncomms8965

2014

Healy, M. E., Chow, J. D. Y., Byrne, F. L., Breen, D. S., Leitinger, N., Li, C., . . . Hoehn, K. L. (2015). Dietary effects on liver tumor burden in mice treated with the hepatocellular carcinogen diethylnitrosamine. JOURNAL OF HEPATOLOGY, 62(3), 599-606. doi:10.1016/j.jhep.2014.10.024

Adamson, S. E., & Leitinger, N. (2014). The role of pannexin1 in the induction and resolution of inflammation. FEBS LETTERS, 588(8), 1416-1422. doi:10.1016/j.febslet.2014.03.009

Mullins, G. R., Wang, L., Raje, V., Sherwood, S. G., Grande, R. C., Boroda, S., . . . Harris, T. E. (2014). Catecholamine-induced lipolysis causes mTOR complex dissociation and inhibits glucose uptake in adipocytes. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 111(49), 17450-17455. doi:10.1073/pnas.1410530111

Desai, B. N., & Leitinger, N. (2014). Purinergic and calcium signaling in macrophage function and plasticity. FRONTIERS IN IMMUNOLOGY, 5. doi:10.3389/fimmu.2014.00580

2013

Leitinger, N., & Schulman, I. G. (2013). Phenotypic Polarization of Macrophages in Atherosclerosis. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 33(6), 1120-1126. doi:10.1161/ATVBAHA.112.300173

2012

Meher, A. K., Sharma, P. R., Lira, V. A., Yamamoto, M., Kensler, T. W., Yan, Z., & Leitinger, N. (2012). Nrf2 deficiency in myeloid cells is not sufficient to protect mice from high-fat diet-induced adipose tissue inflammation and insulin resistance. FREE RADICAL BIOLOGY AND MEDICINE, 52(9), 1708-1715. doi:10.1016/j.freeradbiomed.2012.02.022

Halterman, J. A., Kwon, H. M., Leitinger, N., & Wamhoff, B. R. (2012). NFAT5 expression in bone marrow-derived cells enhances atherosclerosis and drives macrophage migration. FRONTIERS IN PHYSIOLOGY, 3. doi:10.3389/fphys.2012.00313

Lohman, A. W., Weaver, J. L., Billaud, M., Sandilos, J. K., Griffiths, R., Straub, A. C., . . . Isakson, B. E. (2012). S-Nitrosylation Inhibits Pannexin 1 Channel Function. JOURNAL OF BIOLOGICAL CHEMISTRY, 287(47). doi:10.1074/jbc.M112.397976

2011

Adamson, S., & Leitinger, N. (2011). Phenotypic modulation of macrophages in response to plaque lipids. CURRENT OPINION IN LIPIDOLOGY, 22(5), 335-342. doi:10.1097/MOL.0b013e32834a97e4

Kadl, A., Sharma, P. R., Chen, W., Agrawal, R., Meher, A. K., Rudraiah, S., . . . Leitinger, N. (2011). Oxidized phospholipid-induced inflammation is mediated by Toll-like receptor 2. FREE RADICAL BIOLOGY AND MEDICINE, 51(10), 1903-1909. doi:10.1016/j.freeradbiomed.2011.08.026

Rao, J., Elliott, M. R., Leitinger, N., Jensen, R. V., Goldberg, J. B., & Amin, A. R. (2011). RahU: An inducible and functionally pleiotropic protein in Pseudomonas aeruginosa modulates innate immunity and inflammation in host cells. CELLULAR IMMUNOLOGY, 270(2), 103-113. doi:10.1016/j.cellimm.2011.05.012

Rao, J., DiGiandomenico, A., Artamonov, M., Leitinger, N., Amin, A. R., & Goldberg, J. B. (2011). Host derived inflammatory phospholipids regulate rahU (PA0122) Gene, Protein, and Biofilm Formation in Pseudomonas aeruginosa. CELLULAR IMMUNOLOGY, 270(2), 95-102. doi:10.1016/j.cellimm.2011.04.011

Manichaikul, A., Wang, Q., Shi, Y. L., Zhang, Z., Leitinger, N., & Shi, W. (2011). Characterization of Ath29, a major mouse atherosclerosis susceptibility locus, and identification of Rcn2 as a novel regulator of cytokine expression. AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 301(3), H1056-H1061. doi:10.1152/ajpheart.00366.2011

Sharma, R., Sharma, P. R., Kim, Y. -C., Leitinger, N., Lee, J. K., Fu, S. M., & Ju, S. -T. (2011). IL-2-controlled expression of multiple T cell trafficking genes and Th2 cytokines in the regulatory T cell-deficient scurfy mice: implication to multiorgan inflammation and control of skin and lung inflammation (vol 186, pg 1268, 2011). JOURNAL OF IMMUNOLOGY, 186(8), 5012-5013. doi:10.4049/jimmunol.1190010

Sharma, R., Sharma, P. R., Kim, Y. -C., Leitinger, N., Lee, J. K., Fu, S. M., & Ju, S. -T. (2011). IL-2-Controlled Expression of Multiple T Cell Trafficking Genes and Th2 Cytokines in the Regulatory T Cell-Deficient Scurfy Mice: Implication to Multiorgan Inflammation and Control of Skin and Lung Inflammation. JOURNAL OF IMMUNOLOGY, 186(2), 1268-1278. doi:10.4049/jimmunol.1002677

2010

Sharma, R., Sharma, P., Du, Z., & Leitinger, N. (2010). Oxidized phospholopids induce a tolerogenic response that is protective in a Streptozotocin-induced model of type 1 diabetes (T1D). JOURNAL OF IMMUNOLOGY, 184.

Owens, A. P. I. I. I., Barcel, A., Glover, S., Leitinger, N., & Mackman, N. (2010). Oxidized Phospholipids Induce the Expression of Tissue Factor in Human Monocytes via TLR4. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 30(11), E296.

Heberlein, K. R., Straub, A. C., Best, A. K., Greyson, M. A., Looft-Wilson, R. C., Sharma, P. R., . . . Isakson, B. E. (2010). Plasminogen Activator Inhibitor-1 Regulates Myoendothelial Junction Formation. CIRCULATION RESEARCH, 106(6), 1092-1102. doi:10.1161/CIRCRESAHA.109.215723

Gruber, F., Mayer, H., Lengauer, B., Mlitz, V., Sanders, J. M., Kadl, A., . . . Tschachler, E. (2010). NF-E2-related factor 2 regulates the stress response to UVA-1-oxidized phospholipids in skin cells. FASEB JOURNAL, 24(1), 39-48. doi:10.1096/fj.09-133520

Kadl, A., Meher, A. K., Sharma, P. R., Lee, M. Y., Doran, A. C., Johnstone, S. R., . . . Leitinger, N. (2010). Identification of a Novel Macrophage Phenotype That Develops in Response to Atherogenic Phospholipids via Nrf2. CIRCULATION RESEARCH, 107(6), 737-U155. doi:10.1161/CIRCRESAHA.109.215715