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Research Snapshot Theater: Immunology, Adult

Immune Dysregulation in Infants After Cardiopulmonary Bypass

Monday, March 23, 2026
2:30 PM - 3:30 PM Central Time
Location: Connections Central - RST 09

  • Andrew Prout, MD

    Children's Hospital of Michigan, Michigan

    Disclosure(s): No relevant financial relationship(s) to disclose.

  • RD

    Robert Dickson, MD

    Professor of Pulmonary and Critical Care Medicine
    University of Michigan Health System

    Disclosure information not submitted.

  • SS

    Sureyya Savasan, MD

    Professor
    Children's Hospital of Michigan, Central Michigan University College of Medicine

    Disclosure information not submitted.

  • KM

    Kathleen Meert, MD

    Professor and Chair of Department of Pediatrics
    Children's Hospital of Michigan / Central Michigan University, Michigan

    Disclosure information not submitted.

Introduction: Infants with congenital heart disease (CHD) who require cardiopulmonary bypass (CPB) for repair are at high risk for postop infection. Whole blood ex vivo TNF-α production in response to lipopolysaccharide (LPS) and IFN-γ after phytohemagglutinin (PHA) stimulation are measures of immune capacity that predict secondary infection in critical illness. We described the cellular changes associated with diminished immune capacity and postop infection in infants after CPB. We hypothesized that compositional changes in cellular populations and characteristics may be related to diminished immune capacity and postop infection.


Methods: TNF-α levels after LPS and IFN-γ levels after PHA stimulation were measured pre- and postoperatively. Flow cytometry was performed under each condition at each timepoint. Postop infection was defined as positive culture from a sterile site. We defined cellular characteristics associated with impaired cytokine production and postop infection. ChatGPT 4.0 was used for generation of code snippets for data cleaning.


Results: We enrolled 21 infants with CHD after cardiac surgery with CPB, 6 (28.6%) of whom had postop bacterial infection. Twelve (57.1%) had newly impaired TNF-α or IFN-γ production. Cellular features independently associated with impaired TNF-α production included preop CD4+/CD8+ ratio (p=0.008), preop HLA-DR+ monocytes (p=0.02), and postop decline in classical monocytes. Decreased DR+ monocytes after LPS stimulation (p = 0.03) in preop samples were associated with postop infection in univariate analysis. Cellular features were not independently associated with impaired IFN-γ production. Decreased TNF-α or IFN-γ production after stimulation with LPS or PHA were not associated with infection.


Conclusions: Change in expression of HLA-DR on monocytes was associated with postop infection in infants after heart surgery, and was more predictive than cytokine production capacity. Cell population immune phenotypical alterations after ex vivo LPS stimulation may assist in accurate risk stratification for postop infection. Understanding the underlying mechanism of variable immune phenotypic characteristics may lead to interventions that reduce the risk of postop infection in infants after heart surgery.