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The Zingarelli Laboratory is focused on the investigation of the pathophysiologic mechanisms of sepsis, trauma and hemorrhagic shock, which are leading causes of morbidity and mortality in intensive care units. Dr. Zingarelli has identified putative anti-inflammatory nuclear receptors, the peroxisome proliferator activated receptors (PPARγ , PPARα and PPARδ ), and liver X receptors (LXRs), which regulate gene transcription of several cytotoxic modulators and may be important defense factors. Recent research efforts also focus on understanding the role of aging on the clinical course of infections, severe hemorrhage and trauma. The laboratory employs a multidisciplinary approach combining in vivo and in vitro experimental models in genetically modified rodents and cell lines. These models are also utilized as a translational research platform to screen novel pharmacological compounds that can modulate the molecular mechanisms of organ function. The goal is to identify specific therapeutic interventions for pediatric, adult and elderly patients.
The Zingarelli Laboratory is also collaborating with several basic science and translational studies in the Division of Critical Care Medicine. In collaboration with Dr. Hector Wong, the Zingarelli Laboratory investigates novel biomarkers and pathways involved in sepsis pathobiology, including the role of the matrix metallo-proteinase 8 (MMP-8). In collaboration with Dr. Jennifer Kaplan, the Zingarelli Laboratory evaluates the effects of obesity on the increased risk of complications after infections.
Dr. Zingarelli also collaborates on basic science studies with Dr. James A. Cook of the Medical University of South Carolina on the molecular mechanisms by which Gram-negative or Gram-positive bacteria interact with the host cells and mediate the pathological effects of infections.
Ongoing projects are primarily funded by multiple grants from the National Institutes of Health.
Botez G, Piraino G, Hake PW, Ledford JR, O’Connor M, Cook JA, Zingarelli B. Age-dependent therapeutic effects of liver X receptor-α activation in murine polymicrobial sepsis. Innate Immun., 2015 Aug;21(6):609-18.
Hobson M, Hake PW, O’Connor, Schulte C, Moore V, James JM, Piraino G, Zingarelli B. Conditional deletion of cardiomyocyte peroxisome proliferator-activated receptor γ enhances myocardial ischemia-reperfusion injury in mice. Shock. 2014 Jan;41(1):40-7.
Slinko S, Piraino G, Hake PW, Ledford JR, O’Connor M, Wong HR, Zingarelli B. Combined zinc supplementation with proinsulin C-peptide treatment decreases the inflammatory response and mortality in murine polymicrobial sepsis. Shock. 2014 Apr;41(4):292-300.
Wang X, Huang W, Yang Y, Wang Y, Peng T, Chang J, Caldwell CC, Zingarelli B, Fan GC. Loss of MiR-223 duplex (5p and 3p) aggravates myocardial depression and mortality in polymicrobial sepsis. Biochim Biophys Acta. 2014 May;1842(5):701-11.
Osuchowski MF, Remick DG, Lederer JA, Lang CH, Aasen AO, Aibiki M, Azevedo LC, Bahrami S, Boros M, Cooney R, Cuzzocrea S, Jiang Y, Junger WG, Hirasawa H, Hotchkiss RS, Li XA, Radermacher P, Redl H, Salomao R, Soebandrio A, Thiemermann C, Vincent JL, Ward P, Yao YM, Yu HP, Zingarelli B, Chaudry IH. Abandon the Mouse Research Ship? Not Just Yet! Shock. 2014 Jun;41(6):463-75.
Fan H, Goodwin AJ, Chang E, Zingarelli B, Borg K, Guan S, Halushka PV, Cook JA. Endothelial progenitor cells and a stromal cell-derived factor-1α analogue synergistically improve survival in sepsis. Am J Respir Crit Care Med. 2014 Jun 15;189(12):1509-19.
Guan S, Guo C, Zingarelli B, Wang L, Halushka PV, Cook JA, Fan H. Combined treatment with a CXCL12 analogue and antibiotics improves survival and neutrophil recruitment and function in murine sepsis. Immunology. 2014 Sep 8.
Guo F, Li J, Du W, Zhang S, O’Connor M, Thomas G, Kzoma S, Zingarelli B, Pang Q, Zheng Y. mTOR regulates DNA damage response through NF-κB-mediated FANCD2 pathway in hematopoietic cells. Leukemia. 2013 Oct; 27(10):2040-6.
Samraj R, Zingarelli B, Wong HR. Role of biomarkers in sepsis care. Shock. 2013 Nov; 40(5):358-65.
Kaplan JM, Nowell M, Lahni P, Chima RS, Zingarelli B. Pioglitazone reduces inflammation through inhibition of NF-κB in polymicrobial sepsis. Innate Immun. 2014 Jul; 20(5):519-28.
Professor, UC Department of Pediatrics
Director of Basic Science Research, Division of Critical Care Medicine, Cincinnati Children's Hospital Medical Center
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