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Neonatal CD71+ Erythroid Cells Do Not Modify Murine Sepsis Mortality
James L Wynn1, Philip O Scumpia2, Blair T Stocks3
1Division of Neonatology, Department of Pediatrics, Vanderbilt University, Nashville, TN 37232; james.wynn@peds.ufl.edu.
Journal of Immunology (Baltimore, Md. : 1950)
|June 24, 2015
Summary
Neonatal CD71(+) erythroid splenocytes did not impact sepsis survival in mice. Anti-CD71 antibody treatment, not cell reduction, enhanced bacterial clearance, suggesting limited roles for these cells in neonatal immunity.
Area of Science:
- Immunology
- Neonatal Research
- Infectious Disease
Background:
- Sepsis poses a significant threat to neonates globally.
- Previous studies suggested CD71(+) erythroid splenocytes might impair neonatal immune defense.
Purpose of the Study:
- To investigate the role of CD71(+) erythroid splenocytes in neonatal mortality during endotoxin or sepsis challenges.
- To characterize circulating CD71(+) erythroid (CD235a(+)) cells in human neonates.
Main Methods:
- Adoptive transfer and antibody-mediated reduction of CD71(+) erythroid splenocytes in murine models.
- Assessing survival rates after endotoxin and polymicrobial sepsis challenges.
- Characterizing human cord blood CD71(+)CD235a(+) cells and evaluating ex vivo immunosuppression.
Main Results:
- Neither adoptive transfer nor reduction of CD71(+) erythroid splenocytes affected murine neonatal survival to sepsis.
- Anti-CD71 antibody treatment reduced splenic bacterial load in mice.
- Human CD71(+)CD235a(+) cells in cord blood were identified as reticulocytes.
Conclusions:
- CD71(+) erythroid splenocytes appear to have a limited impact on murine neonatal sepsis survival under the tested conditions.
- Enhanced bacterial clearance in anti-CD71 antibody-treated mice was likely due to immune priming, not cell reduction.
- The rapid postnatal decrease in human reticulocytes suggests a potentially limited role in neonatal inflammation control.
