Research Topics
Species | K J TraceySummaryAffiliation: Highway Safety North Country: USA Publications
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Publications
The vagus nerve and nicotinic receptors modulate experimental pancreatitis severity in miceDavid J van Westerloo
Laboratory of Experimental Internal Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
Gastroenterology 130:1822-30. 2006..This anti-inflammatory effect is mediated by an interaction of acetylcholine, the principal neurotransmitter of the vagus nerve, with macrophage cholinergic nicotinic receptors expressing the alpha7 subunit...- Mind over immunityK J Tracey
Laboratory of Biomedical Science, North Shore University Hospital, New York University, Manhasset, New York 11030, USA
FASEB J 15:1575-6. 2001..This newly appreciated cholinergic anti-inflammatory pathway provides a neural substrate to study brain-immune interactions and might be harnessed for therapy of cytokine-mediated disease... 
Pharmacological stimulation of the cholinergic antiinflammatory pathwayThomas R Bernik
Laboratory of Biomedical Science, North Shore-LIJ Research Institute, 350 Community Drive, Manhasset, NY 11030, USA
J Exp Med 195:781-8. 2002..Together, these results indicate that stimulation of the cholinergic antiinflammatory pathway by either pharmacological or electrical methods can attenuate the systemic inflammatory response to endotoxin-induced shock...- The inflammatory reflexKevin J Tracey
Laboratory of Biomedical Science, North Shore LIJ Research Institute, Manhasset, New York 11030, USA
Nature 420:853-9. 2002..The opportunity now exists to apply this insight to the treatment of inflammation through selective and reversible 'hard-wired' neural systems... - The cholinergic anti-inflammatory pathwayValentin A Pavlov
Laboratory of Biomedical Science, Institute for Medical Research North Shore LIJ Health System, Manhasset, NY 11030, USA
Brain Behav Immun 19:493-9. 2005..We also discuss possible clinical implications of vagus nerve stimulation and cholinergic modalities in the treatment of inflammatory diseases... - Lethal weight loss: the focus shifts to signal transductionKevin J Tracey
North Shore Long Island Jewish Research Institute, Manhasset, NY 11020, USA
Sci STKE 2002:pe21. 2002..Furthermore, soluble factors including TNF and proteolysis-inducing factor may enhance protein degradation through the ubiquitin-proteosome pathway... - HMG-1 as a late mediator of endotoxin lethality in miceH Wang
Department of Emergency Medicine and Department of Surgery, North Shore University Hospital New York University School of Medicine, Manhasset, NY 11030, USA
Science 285:248-51. 1999..Septic patients who succumbed to infection had increased serum HMG-1 levels, suggesting that this protein warrants investigation as a therapeutic target... - Role of vagus nerve signaling in CNI-1493-mediated suppression of acute inflammationL V Borovikova
The Picower Institute for Medical Research, Manhasset, NY 11030, USA
Auton Neurosci 85:141-7. 2000..These results now identify a previously unrecognized role of efferent vagus nerve activity in mediating the central action of an anti-inflammatory agent... 
Cholinergic control of inflammationM Rosas-Ballina
The Feinstein Institute for Medical Research, North Shore LIJ Health System, Manhasset, NY 11030, USA
J Intern Med 265:663-79. 2009..We discuss potential therapeutic applications to treat diseases characterized by acute or chronic inflammation, including autoimmune diseases, and propose future research directions...- Spermine inhibition of monocyte activation and inflammationM Zhang
The Picower Institute for Medical Research, Manhasset, New York 11030, USA
Mol Med 5:595-605. 1999..Administration of BAP in vivo significantly augmented the development of carrageenan-induced paw edema and nitric oxide release. Thus, endogenous spermine normally inhibits the innate inflammatory response by restraining macrophages... - Fetuin (alpha2-HS-glycoprotein) opsonizes cationic macrophagedeactivating moleculesH Wang
Department of Emergency Medicine, North Shore University Hospital New York University School of Medicine, Manhasset, NY 11030, USA
Proc Natl Acad Sci U S A 95:14429-34. 1998..g., spermine) and pharmacologic (e.g., CNI-1493). This role of fetuin as an opsonic participant in macrophage-deactivating mechanisms has implications for understanding and manipulating the innate immune response... - HMG-1 rediscovered as a cytokineH Yang
Laboratory of Biomedical Science, North Shore University Hospital, Manhasset, New York 11030, USA
Shock 15:247-53. 2001..When released by activated monocytes, it participates in the development of lethality and it activates downstream cytokine release. This review covers the general features of HMG-1 and its newly appreciated role as a cytokine... - Fetuin, a negative acute phase protein, attenuates TNF synthesis and the innate inflammatory response to carrageenanM Ombrellino
Department of Surgery, North Shore University Hospital-New York University School of Medicine, Manhasset, New York 11030, USA
Shock 15:181-5. 2001..These results now reveal a previously unrecognized anti-inflammatory role of fetuin in counter-regulating the innate immune response, and suggest that it may be possible to use fetuin as an experimental anti-inflammatory agent... - Autonomic neural regulation of immunityC J Czura
North Shore LIJ Research Institute, Center for Patient Oriented Research, Manhasset, NY, USA
J Intern Med 257:156-66. 2005..The description of the cholinergic anti-inflammatory now brings to the fore several new therapeutic strategies for inflammatory disease, and suggests that many of these diseases may actually be diseases of autonomic dysfunction... - CNI-1493 attenuates hemodynamic and pro-inflammatory responses to LPSP E Molina
Department of Surgery, North Shore University Hospital, Manhasset, New York 11030, USA
Shock 10:329-34. 1998..These results suggest diverse effects of CNI-1493 that are tissue specific and that confer protection against the hemodynamic and inflammatory responses to LPS... - Prevention and treatment of experimental autoimmune encephalomyelitis by CNI-1493, a macrophage-deactivating agentJ A Martiney
The Picower Institute for Medical Research, Manhasset, NY 11030, USA
J Immunol 160:5588-95. 1998..Moreover, drug treatment during the chronic phase resulted in amelioration of clinical signs. The data presented here should prove useful in developing novel chemotherapeutic approaches for the treatment of MS... - Extracellular role of HMGB1 in inflammation and sepsisH Wang
Laboratory of Emergency Medicine, North Shore LIJ Research Institute, Manhasset, NY 11030, USA
J Intern Med 255:320-31. 2004..Strategies to inhibit HMGB1 activity and release are being investigated in these and other preclinical models of acute and chronic inflammation... - Neural regulators of innate immune responses and inflammationV A Pavlov
Laboratory of Biomedical Science, North Shore-LIJ Research Institute, 350 Community Drive, Manhasset, New York 11030, USA
Cell Mol Life Sci 61:2322-31. 2004..The clinical implications of the recently discovered anti-inflammatory role of the efferent vagus nerve are also discussed... - Dual roles for HMGB1: DNA binding and cytokineC J Czura
Laboratory of Biomedical Science, North Shore/Long Island Jewish Research Institute, Manhasset, New York 11030, USA
J Endotoxin Res 7:315-21. 2001..The delayed kinetics of HMGB1 release indicate that it may be useful to target this toxic cytokine in the development of future therapies... - Controlling inflammation: the cholinergic anti-inflammatory pathwayV A Pavlov
Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY 11030, USA
Biochem Soc Trans 34:1037-40. 2006.... - Cholinergic agonists attenuate renal ischemia-reperfusion injury in ratsM M Yeboah
Laboratory of Medicinal Biochemistry, The Feinstein Institute for Medical Research, North Shore LIJ Health System, Manhasset, New York 11030, USA
Kidney Int 74:62-9. 2008..Cholinergic stimulation significantly decreased tubular necrosis in vagotomized rats after injury, implying an intact vagus nerve is not required for this renoprotective effect... - Vagus nerve stimulation attenuates the systemic inflammatory response to endotoxinL V Borovikova
The Picower Institute for Medical Research, Manhasset, New York 11030, USA
Nature 405:458-62. 2000..Direct electrical stimulation of the peripheral vagus nerve in vivo during lethal endotoxaemia in rats inhibited TNF synthesis in liver, attenuated peak serum TNF amounts, and prevented the development of shock... - Cholinergic stimulation blocks endothelial cell activation and leukocyte recruitment during inflammationRubina W Saeed
Laboratory of Medicinal Biochemistry, Institute for Medical Research at North Shore LIJ, Manhasset, NY 11030, USA
J Exp Med 201:1113-23. 2005..These findings identify the endothelium, a key regulator of leukocyte trafficking during inflammation, as a target of anti-inflammatory cholinergic mediators... - Cholinergic antiinflammatory pathway inhibition of tumor necrosis factor during ischemia reperfusionThomas R Bernik
Division of Vascular Surgery, North Shore University, 300 Community Drive, Manhasset, NY 11030, USA
J Vasc Surg 36:1231-6. 2002..02). CONCLUSION: VNS significantly attenuates TNF synthesis and shock during reperfusion injury in a standard model of aortic occlusion. Clinical evaluation of VNS for this condition may be warranted... - Nicotinic acetylcholine receptor alpha7 subunit is an essential regulator of inflammationHong Wang
Laboratory of Biomedical Science, North Shore Long Island Jewish Research Institute, 350 Community Drive, Manhasset, New York 11030, USA
Nature 421:384-8. 2003..Thus, the nicotinic acetylcholine receptor alpha7 subunit is essential for inhibiting cytokine synthesis by the cholinergic anti-inflammatory pathway... - Transcutaneous vagus nerve stimulation reduces serum high mobility group box 1 levels and improves survival in murine sepsisJared M Huston
Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, Manhasset, NY 11030, USA
Crit Care Med 35:2762-8. 2007..Here we developed a method of transcutaneous mechanical vagus nerve stimulation and then investigated whether this therapy can protect mice against sepsis lethality... - Elevated high-mobility group box 1 levels in patients with cerebral and myocardial ischemiaRichard S Goldstein
Department of Emergency Medicine, North Shore University Hospital, North Shore LIJ, Manhasset, NY 11030, USA
Shock 25:571-4. 2006..8+/-10.9 ng/mL, vs. cerebral ischemia serum HMGB1, 218+/-18.8 ng/mL; P<0.001). These results suggest that systemic HMGB1 levels are elevated in human ischemic disease... - Role of HMGB1 in apoptosis-mediated sepsis lethalityShixin Qin
Critical Therapeutics, Inc, Lexington, MA 02421, USA
J Exp Med 203:1637-42. 2006..Thus, our data indicate that HMGB1 production is downstream of apoptosis on the final common pathway to organ damage in severe sepsis... - HMGB1 activates replication of latent HIV-1 in a monocytic cell-line, but inhibits HIV-1 replication in primary macrophagesPiotr Nowak
Division of Clinical Virology, Karolinska Institutet, Karolinska University Hospital Huddinge, Stockholm, Sweden
Cytokine 34:17-23. 2006..Our data suggest that extracellular HMGB1 has a dichotomic effect on the HIV-1 infection in monocytes but not in lymphocytes. Both activation of latent HIV-1 infection and inhibition of active replication can thus be seen in vitro... - HMGB1 is a bone-active cytokineJieping Yang
Department of Anatomy and Cell Biology, Indiana University School of Medicine, Indianapolis, Indiana 46202, USA
J Cell Physiol 214:730-9. 2008..Our data suggest that apoptotic bone cells release HMGB1, that within the marrow HMGB1 is a bone resorption signal, and that intramembraneous and endochondral osteoblasts exhibit differential responses to this cytokine... - High mobility group box 1 (HMGB1)Huan Yang
Laboratory of Biomedical Sciences, Institute for Medical Research, North Shore-Long Island Jewish Health System, Manhasset, NY, USA
Crit Care Med 33:S472-4. 2005 - Fat meets the cholinergic antiinflammatory pathwayKevin J Tracey
North Shore LIJ Research Institute, Manhassset, NY 11030, USA
J Exp Med 202:1017-21. 2005..Here we discuss this new data and its potential implications for dietary intervention in the treatment of inflammatory diseases... - Suppressor alphabeta T lymphocytes control innate resistance to endotoxic shockJessica Jones-Carson
Departments of Medicine, and Microbiology, University of Colorado Health Sciences Center, Denver, USA
J Infect Dis 192:1039-46. 2005..These observations suggest that suppressor alphabeta T lymphocytes protect against the proinflammatory cascade unleashed during the innate stages of endotoxemia... - Splenic nerve is required for cholinergic antiinflammatory pathway control of TNF in endotoxemiaMauricio Rosas-Ballina
Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY 11030, USA
Proc Natl Acad Sci U S A 105:11008-13. 2008.... - Modulation of TNF release by choline requires alpha7 subunit nicotinic acetylcholine receptor-mediated signalingWilliam R Parrish
Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, North Shore LIJ Health System, Manhasset, New York 11030, USA
Mol Med 14:567-74. 2008..Collectively, these data characterize the anti-inflammatory efficacy of choline and demonstrate that the modulation of TNF release by choline requires alpha7nAChR-mediated signaling... - From CNI-1493 to the immunological homunculus: physiology of the inflammatory reflexStacey L Oke
Feinstein Institute for Medical Research, North Shore LIJ Health System, 350 Community Drive, Manhasset, NY 11030, USA
J Leukoc Biol 83:512-7. 2008..Receptor-ligand engagement suppresses proinflammatory cytokines and prevents tissue damage. Herein is a review of some of the experimental studies that define the inflammatory reflex and its anatomic and physiologic components... - Systemic inflammation and remote organ injury following trauma require HMGB1Ryan M Levy
Dept of Surgery, F 1200 PUH, Univ of Pittsburgh, 200 Lothrop St, Pittsburgh, PA 15213, USA
Am J Physiol Regul Integr Comp Physiol 293:R1538-44. 2007..Collectively, these data demonstrate a critical role for a TLR4-HMGB1 pathway in the initiation of systemic inflammation and end-organ injury following isolated peripheral tissue injury... - Aerobic exercise attenuates inducible TNF production in humansRichard P Sloan
Division of Behavioral Medicine, Department of Psychiatry, Columbia University, New York, NY 10032, USA
J Appl Physiol 103:1007-11. 2007..001) decreases in TNF release only in the H group. These data suggest that in healthy young adults, a 12-wk high-intensity aerobic training program downregulates blood monocyte production of stimulated cytokine release... - Cholinergic anti-inflammatory pathway activity and High Mobility Group Box-1 (HMGB1) serum levels in patients with rheumatoid arthritisRichard S Goldstein
The Feinstein Institute for Medical Research, and Department of Emergency Medicine, North Shore University Hospital, Manhasset, NY 11030, USA
Mol Med 13:210-5. 2007.... - RR interval variability is inversely related to inflammatory markers: the CARDIA studyRichard P Sloan
Behavioral Medicine Program, Department of Psychiatry, Columbia University Medical Center, New York, NY 10032, USA
Mol Med 13:178-84. 2007..These findings are consistent with the hypothesis that diminished descending vagal anti-inflammatory signals can allow cytokine overproduction in humans... - Selective alpha7-nicotinic acetylcholine receptor agonist GTS-21 improves survival in murine endotoxemia and severe sepsisValentin A Pavlov
Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, Manhasset, NY, USA
Crit Care Med 35:1139-44. 2007..Here we studied whether GTS-21, a selective alpha7-nicotinic acetylcholine receptor agonist, inhibits proinflammatory cytokines in vitro and in vivo and improves survival in murine endotoxemia and severe sepsis... - Physiology and immunology of the cholinergic antiinflammatory pathwayKevin J Tracey
The Feinstein Institute for Medical Research, Manhasset, New York 11030, USA
J Clin Invest 117:289-96. 2007..Herein is a review of this physiological, functional anatomical mechanism for neurological regulation of cytokine-dependent disease that begins to define an immunological homunculus... - High mobility group B1 protein suppresses the human plasmacytoid dendritic cell response to TLR9 agonistsPetar J Popovic
Division of Surgical Oncology, Department of Surgery and Molecular Medicine Institute, University of Pittsburgh, Pittsburgh, PA 15232, USA
J Immunol 177:8701-7. 2006..Our observations suggest that HMGB1 may play a critical role in regulating the immune response during chronic inflammation and tissue damage through modulation of PDC function... - HMGB1 signals through toll-like receptor (TLR) 4 and TLR2Man Yu
Laboratories of Biomedical Science, The Feinstein Institute for Medical Research, Manhasset, NY 11030, USA
Shock 26:174-9. 2006..Taken together, our data suggest that there is a differential usage of TLR2 and TLR4 in HMGB1 signaling in primary cells and in established cell lines, adding complexity to studies of HMGB1 signaling which was not previously expected... - Central muscarinic cholinergic regulation of the systemic inflammatory response during endotoxemiaValentin A Pavlov
Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY 11030, USA
Proc Natl Acad Sci U S A 103:5219-23. 2006..The role of central muscarinic receptors in activating the cholinergic antiinflammatory pathway is of interest for the use of centrally acting muscarinic cholinergic enhancers as antiinflammatory agents... - It takes nerve to dampen inflammationChristine N Metz
Nat Immunol 6:756-7. 2005 - The cholinergic anti-inflammatory pathway regulates the host response during septic peritonitisDavid J van Westerloo
Laboratory of Experimental Internal Medicine and Department of Gastroenterology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands
J Infect Dis 191:2138-48. 2005..This anti-inflammatory effect is mediated by an interaction between acetylcholine, the principal neurotransmitter of the vagus nerve, and cholinergic nicotinic acetylcholine receptors on macrophages... - The cholinergic anti-inflammatory pathway: a missing link in neuroimmunomodulationValentin A Pavlov
Laboratory of Biomedical Science, North Shore LIJ-Research Institute, Manhasset, NY 11030, USA
Mol Med 9:125-34. 2003..The clinical implications of this novel mechanism also are discussed... - High mobility group box-1 as a therapeutic target downstream of tumor necrosis factorChristopher J Czura
Laboratory of Biomedical Science, North Shore-Long Island Jewish Research Institute, Manhasset, New York 11030, USA
J Infect Dis 187:S391-6. 2003..It will now be important to determine whether this wider window of activity can be translated into therapeutic advantage for human inflammatory disease... - Structural basis for the proinflammatory cytokine activity of high mobility group box 1Jianhua Li
Laboratory of Biomedical Science, North Shore-Long Island Jewish Research Institute, 350 Community Drive, Manhasset, NY 11030, USA
Mol Med 9:37-45. 2003..These results indicate that a proinflammatory domain of HMGB1 maps to the highly conserved DNA-binding B box, making this primary sequence a suitable target in the design of therapeutics... - HMGB1 as a cytokine and therapeutic targetHuan Yang
Laboratory of Biomedical Science, North Shore Long Island Jewish Research Institute, Manhasset, New York 11030, USA
J Endotoxin Res 8:469-72. 2002..Thus, strategies that target HMGB1 with specific antibodies or antagonists have potential for treating lethal systemic inflammatory diseases characterized by excessive HMGB1 release... - The gesture life of high mobility group box 1Steven G Friedman
Division of Vascular Surgery, North Shore University Hospital, North Shore-Long Island Jewish Research Institute, Manhasset, New York, USA
Curr Opin Clin Nutr Metab Care 6:283-7. 2003.... - IFN-gamma induces high mobility group box 1 protein release partly through a TNF-dependent mechanismBeatriz Rendon-Mitchell
Center of Immunology and Inflammation, North Shore-Long Island Jewish Research Institute, Manhasset, NY 11030, USA
J Immunol 170:3890-7. 2003..These data suggest that IFN-gamma plays an important role in the regulation of HMGB1 release through a TNF- and Janus kinase 2-dependent mechanism... - Targeting high mobility group box 1 as a late-acting mediator of inflammationChristopher J Czura
Laboratory of Biomedical Science, North Shore-LIJ Research Institute, 350 Community Drive, Manhasset, NY 11030, USA
Crit Care Med 31:S46-50. 2003..A candidate mediator of delayed lethality is high mobility group box 1, a cellular and nuclear protein that is now recognized as a cytokine and experimental therapeutic target... - HMGB1 as a DNA-binding cytokineUlf Andersson
Department of Medicine, Rheumatology Research Unit, Karolinska Hospital, Stockholm, Sweden
J Leukoc Biol 72:1084-91. 2002.... - Ethyl pyruvate prevents lethality in mice with established lethal sepsis and systemic inflammationLuis Ulloa
Laboratory of Biomedical Science, North Shore-LIJ Research Institute, 350 Community Drive, Manhasset, NY 11030, USA
Proc Natl Acad Sci U S A 99:12351-6. 2002..EP now warrants further evaluation as an experimental "rescue" therapeutic for sepsis and other potentially fatal systemic inflammatory disorders... - HMGB-1, a DNA-binding protein with cytokine activity, induces brain TNF and IL-6 production, and mediates anorexia and taste aversionDavide Agnello
Laboratory of Neuroimmunology, Mario Negri Institute for Pharmacological Research, 20157 Milano, Italy
Cytokine 18:231-6. 2002..In a model of endotoxemia, passive immunization with anti-HMG-1 antibodies attenuated the development of hypophagia, indicating that HMG-1 is a mediator of sickness behaviour associated with endotoxemia... - Further characterization of high mobility group box 1 (HMGB1) as a proinflammatory cytokine: central nervous system effectsKevin A O'Connor
Department of Psychology and Center for Neuroscience, University of Colorado, Boulder, CO 80309, USA
Cytokine 24:254-65. 2003..Nonetheless, these data suggest that HMGB1 may play a role as an endogenous pyrogen and support the concept that HMGB1 has proinflammatory characteristics within the central nervous system... - HMGB1 in sepsisUlf Andersson
Department of Woman and Child Health, Karolinska Institutet, Astrid Lindgren Children s Hospital, Stockholm, Sweden
Scand J Infect Dis 35:577-84. 2003..Effectiveness of delayed treatment with HMGB1 blockade up to 24 h after induction of experimental sepsis offers a unique window of opportunities to allow rescue from lethal sepsis... - Persistent elevation of high mobility group box-1 protein (HMGB1) in patients with severe sepsis and septic shockJonas Sunden-Cullberg
Department of Medicine, Center for Infectious Medicine, Karolinska Institute at Karolinska University Hospital Huddinge, Stockholm, Sweden
Crit Care Med 33:564-73. 2005.... - The cytokine activity of HMGB1Huan Yang
Laboratory of Biomedical Science, Institute for Medical Research at North Shore Long Island Jewish System, Manhasset, NY 11030, USA
J Leukoc Biol 78:1-8. 2005..Finally, the therapeutic potential of blocking HMGB1 in the treatment of inflammatory diseases is discussed... - Adrenomedullin and its binding protein attenuate the proinflammatory response after hemorrhageXiaoxuan Cui
Division of Surgical Research, North Shore University Hospital and Long Island Jewish Medical Center, Manhasset, NY, USA
Crit Care Med 33:391-8. 2005.... - Suppression of HMGB1 release by stearoyl lysophosphatidylcholine:an additional mechanism for its therapeutic effects in experimental sepsisGuoqian Chen
Department of Emergency Medicine, North Shore University Hospital, New York University School of Medicine, Manhasset, NY 11030, USA
J Lipid Res 46:623-7. 2005..Thus, stearoyl LPC confers protection against lethal experimental sepsis partly by facilitating the elimination of the invading pathogens and partly by inhibiting endotoxin-induced release of a late proinflammatory cytokine, HMGB1... - Ethanol blocks leukocyte recruitment and endothelial cell activation in vivo and in vitroRubina W Saeed
Laboratories of Medical Biochemistry, North Shore-Long Island Jewish Research Institute, 350 Community Drive, Manhasset, NY 11030, USA
J Immunol 173:6376-83. 2004.... - Cholinergic agonists inhibit HMGB1 release and improve survival in experimental sepsisHong Wang
The Center for Immunology and Inflammation, North Shore-LIJ Research Institute, North Shore University Hospital, 350 Community Drive, Manhasset, New York 11030, USA
Nat Med 10:1216-21. 2004.... - Bacterial endotoxin stimulates macrophages to release HMGB1 partly through CD14- and TNF-dependent mechanismsGuoqian Chen
Department of Emergency Medicine, North Shore University Hospital, New York University School of Medicine, 350 Community Drive, Manhasset, NY 11030, USA
J Leukoc Biol 76:994-1001. 2004..g., 10 ng/ml). Taken together, these data suggest that LPS stimulates macrophages to release HMGB1 partly through CD14- and TNF-dependent mechanisms... - HMGB1 in the immunology of sepsis (not septic shock) and arthritisChristopher J Czura
Laboratory of Biomedical Science, North Shore-LIJ Research Institute, Manhasset, New York, USA
Adv Immunol 84:181-200. 2004 - Human genetics: an inflammatory issueKevin J Tracey
Nature 429:35-7. 2004 - Neural inhibition of inflammation: the cholinergic anti-inflammatory pathwayChristopher J Czura
Laboratory of Biomedical Science, North Shore-LIJ Research Institute, Manhasset, NY 11030, USA
J Endotoxin Res 9:409-13. 2003..This newly identified physiological mechanism of maintaining immunological homeostasis suggests that novel therapeutics may effectively modulate inflammatory responses by activating the cholinergic anti-inflammatory pathway... - Globin attenuates the innate immune response to endotoxinHuan Yang
Laboratory of Biomedical Science, North Shore University Hospital-New York University School of Medicine, New York 11030, USA
Shock 17:485-90. 2002..Thus, the heme-iron moiety of hemoglobin, and not the binding of LPS to globin, enhanced macrophage responses to LPS...