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Photo of Steven McElroy

Steven McElroy

Assistant Professor,  Pediatrics

Contact Information

Assistant Professor
1270A CBRB
Iowa City, IA 52242

Phone: +1 319 335 9623
Email: steven-mcelroy@uiowa.edu
Web: McElroy Lab Homepage

Education

BS, Biology/Pre-Medicine, Juniata College
MD, Medicine, Hahnemann School of Medicine (Drexel)
Residency, Pediatrics, St. Christopher's Hospital for Children
Fellowship, Neonatal-Perinatal Medicine, Vanderbilt University

Appointments

Primary: Pediatrics

Centers and Program Affiliations


Research Interests


MeSH Terms from Publications

Receptors, Tumor Necrosis Factor, Type I, Paneth Cells, Infant, Premature, Mucin-3, Enterocolitis, Necrotizing, Goblet Cells, Infant, Newborn, Philadelphia, Mucin-2, Proto-Oncogene Proteins c-ets, Balloon Occlusion, Parturition, Tumor Necrosis Factor-alpha, Receptors, Tumor Necrosis Factor, Type II, Community-Institutional Relations, Phosphorylation, Proto-Oncogene Proteins c-raf, Intubation, Mice, Spectroscopy, Near-Infrared, Splanchnic Circulation, Oximetry, Mucins, Mucus, Renal Circulation

Research Summary

Our work is focused on the mechanisms of gastrointestinal epithelial celI injury and repair during development, especially as it relates to neonatal necrotizing enterocolitis (NEC).  NEC is the single most devastating cause of gastrointestinal mortality and morbidity in premature infants. NEC affects over 4000 infants every year in the United States and carries a mortality of 30% in those affected. Although NEC was first recognized in the1960’s, the medical treatments and mortality are essentially unchanged since that time.  The incidence of NEC is greatest in the most premature babies, suggesting that susceptibility is a consequence of incomplete gut development.  The leading hypothesis for the pathophysiology of NEC is that bacteria normally confined to the intestinal lumen penetrate the immature intestinal epithelial barrier defenses. This leads to invasion of the epithelium and underlying lamina propria, resulting in an exaggerated inflammatory response and tissue destruction. Bacterial invasion is normally prevented by intestinal innate immune components, but this defense system is immature in preterm infants, and may be further diminished during episodes of inflammation.

 

The long-term goal of our lab is to better understand how different gastrointestinal developmental stages differ in their response to inflammation, and specifically the mechanism by which immaturity of the small intestine predisposes development of NEC.  To accomplish this, we are actively examining the effects of inflammation on intestinal homeostasis and repair mechanisms at different stages of intestinal development in mice.  Mice provide an excellent model for studying intestinal development.  Mice and human intestine develop in a defined, sequential pattern.  Newborn mice have small intestine that is developmentally similar to human infants at approximately 16 weeks, and mice at four weeks of age are developmentally similar to term human infants.  Thus examining mice at various points during their first four weeks of life are allowing us to better understand how inflammation affects the intestines of premature infants.

 

We have also discovered that infants with NEC have significantly decreased numbers of Paneth cells. Paneth cells are located at the base of intestinal crypts and are a key cellular component of the innate immune system.  Paneth cells are important in mucosal development, host defense, and regulation of the intestinal microbiota, and maintenance of intestinal stem cell populations.  However, their role in NEC is unknown.  We have developed a novel model of NEC that uses Paneth cell ablation to induce intestinal pathology that is consistent with human NEC. Using this model, we are examining the role of Paneth cells in development of NEC.



Recent Publications


Show publications
  1. Zhang C, Sherman MP, Prince LS, Bader D, Weitkamp JH, Slaughter JC, McElroy SJ.  Paneth cell ablation in the presence of Klebsiella pneumoniae induces necrotizing enterocolitis (NEC)-like injury in immature murine small intestine.  Dis Model Mech. 2012 Feb 10. [Epub ahead of print]
  2. McNeill, S, Gatenby, J C, McElroy, S, Engelhardt, B. Normal cerebral, renal and abdominal regional oxygen saturations using near-infrared spectroscopy in preterm infants. J Perinatol 31(1):51-7, 2011. [PubMed]
  3. McElroy, S, Prince, L, Weitkamp, J, Reese, J, Slaughter, J, Polk, D. Tumor necrosis factor receptor 1-dependent depletion of mucus in immature small intestine: a potential role in neonatal necrotizing enterocolitis. Am J Physiol Gastrointest Liver Physiol 301(4):G656-66, 2011. [PubMed]
  4. McElroy SJ, Weitkamp JH.  “The importance of innate immunicty in the small intestine of the premature infant” Neoreviews. Sept. 2011.  12:517-526.

  5. Edelblum, K, Goettel, J, Koyama, T, McElroy, S, Yan, F, Polk, D. TNFR1 promotes tumor necrosis factor-mediated mouse colon epithelial cell survival through RAF activation of NF-kappaB. J Biol Chem 283(43):29485-94, 2008. [PubMed]
  6. McElroy, S, Frey, M, Yan, F, Edelblum, K, Goettel, J, John, S, Polk, D. Tumor necrosis factor inhibits ligand-stimulated EGF receptor activation through a TNF receptor 1-dependent mechanism. Am J Physiol Gastrointest Liver Physiol 295(2):G285-93, 2008. [PubMed]
  7. McElroy, S, Pietsch, J, Reese, J. Foley catheter tamponade of intercostal hemorrhage in preterm infants. J Pediatr 145(2):241, 2004. [PubMed]
  8. Streeter, K J, McElroy, S J, Zarro, V. Enhanced skill building. Acad Med 72(5):438, 1997. [PubMed]
  9. Epidermal growth factor receptor inhibits colitis-associated cancer in mice.

    Dubé PE, Yan F, Punit S, Girish N, McElroy SJ, Washington MK, Polk DB.

    J Clin Invest. 2012 Jul 9. pii: 62888. doi: 10.1172/JCI62888. [Epub ahead of print]

    PMID:
    22772467
    [PubMed - as supplied by publisher]