SYSTEM OUTAGE: Lurie Children’s continues to respond to a cybersecurity matter. During this time, Stanley Manne Children’s Research Institute continues to conduct research, including recruiting and accepting research participants, collecting data, conducting research procedures, and maintaining research operations. Questions about participation in research, or research in general, may be sent to researchcompliance@luriechildrens.org.

More Information

Research Interests

  • Influenza
  • Respiratory Syncytial Virus
  • Severe Acute Respiratory Syndrome Coronavirus 2
  • Innate Immunity
  • Children
  • Lung Injury

Biography

  • Attending Physician, Critical Care Medicine, Ann & Robert H. Lurie Children’s Hospital of Chicago
  • Crown Family Research Scholar in Developmental Biology, Ann & Robert H. Lurie Children’s Hospital of Chicago
  • Assistant Professor, Department of Pediatrics, Northwestern University Feinberg School of Medicine

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Education and Background

  • Fellowship In Critical Care Medicine, Children's Memorial Hospital, Northwestern University Feinberg School of Medicine
  • Residency In Pediatrics, Children's Memorial Hospital, Northwestern University Feinberg School of Medicine
  • MD, University of Washington School of Medicine 2005
  • Princeton University 2001

Research Highlights

PATHOPHYSIOLOGY OF INFLUENZA A VIRUS-INDUCED LUNG INJURY IN JUVENILES 

Recent clinical data thwart the long-standing dogma that children with influenza have increased morbidity and mortality due to impaired viral clearance. Preliminary data from Dr. Coates and her research team identify an altered innate immune response in IAV-infected juvenile mice as a critical parameter in disease progression. Specifically, they show that increased lung injury in IAV-infected juvenile mice is associated with robust activation of the NOD-like receptor (NLR) protein NLRP3, resulting in increased IFNa/b and IL-1b/18 levels that persist beyond viral elimination. In addition, juvenile lungs produce more MCP-1 and recruit more inflammatory monocytes during IAV infection, which perpetuates NLRP3 activation. Dr. Coates and her research team observe that juvenile recruited monocytes are uniquely inflammatory, and prevention of their recruitment during IAV infection protects juvenile mice from IAV-mediated lung injury. They hypothesize that age-specific, cell autonomous differences in the innate immune response to IAV contribute to the robust and sustained activation of the NLRP3 inflammasome and exacerbate IAV-induced lung injury in juvenile mice. 

NASAL EPITHELIAL GENE EXPRESSION AND SUSCEPTIBILITY TO VIRAL PNEUMONIA IN CHILDREN 

Viral pneumonia is a leading cause of hospitalization in children less than 5 years of age. While influenza virus and respiratory syncytial virus frequently cause viral pneumonia in young children, the novel coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), only rarely causes viral pneumonia in children. Why young children are so much more likely to develop severe influenza virus and respiratory syncytial virus infections, and so much less likely to develop severe SARS-CoV-2 infections, is unknown. Analysis of transcriptional profiles in nasal samples obtained by nearly painless curettage can reveal important information about the host response to viral infections. The nasal epithelium is the first line of defense against viral respiratory infections and may dictate downstream inflammatory and antiviral responses. In children with respiratory syncytial virus infection, Dr. Coates and her research team found a transcriptional signature in nasal samples at the time of admission that was associated with infection outcomes, including duration of oxygen dependence and intensive care unit stay. Therefore, analysis of the host response to influenza virus, respiratory syncytial virus, and SARS-CoV-2 in nasal samples may reveal alterations in gene expression that determine resilience and susceptibility to viral pneumonia. 

Featured Grants

Cross-reactive T Cells and Severity of Illness in SARS-CoV-2 Infection in Children and Adults

American Lung Association
09/01/2021 → 08/31/2023

Using the Nasal Transcriptome to Define COVID-19 Susceptibility in Children and Adults

The American Thoracic Society
02/01/2021 → 01/31/2022

Pathophysiology of Influenza A Virus-induced Lung Injury in Juveniles

National Institutes of Health/National Heart, Lung, and Blood Institute
08/06/2018 → 06/30/2022

A Phase 3 Randomized Controlled Trial of AZM for RSV-induced Respiratory Failure in Children

National Institutes of Health/UAB subcontract
07/01/2021 → 06/30/2025

Mechanisms of Recovery from Viral Pneumonia

NIH/NU
07/01/2021 → 06/30/2026

Immunobiology of Influenza Virus-related Critical Illness in Young Hosts

National Institutes of Health/National Institute of Allergy and Infectious Diseases
09/18/2020 → 08/31/2024

Overcoming COVID-19 Studies

Centers for Disease Control and Prevention
04/01/2020 → 03/31/2022

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