Journal
JOURNAL OF IMMUNOLOGY
Volume 195, Issue 3, Pages 1064-1070Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1500771
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Funding
- Vanderbilt Clinical and Translational Science (CTSA) Award National Center for Advancing Translational Sciences [UL1 TR000445]
- Vanderbilt CTSA Grant from the National Center for Research Resources (National Institutes of Health) [UL1 RR024975-01]
- Eunice Kennedy Shriver National Institute of Child Health and Human Development [T32HD068256, HD061607]
- National Institutes of Health [DK090146, GM106143]
- National Institutes of Health Medical Scientist Training Program [5T32GM007347-33]
- Department of Pediatrics, Vanderbilt University
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Sepsis is a major cause of neonatal mortality and morbidity worldwide. A recent report suggested that murine neonatal host defense against infection could be compromised by immunosuppressive CD71(+) erythroid splenocytes. We examined the impact of CD71(+) erythroid splenocytes on murine neonatal mortality to endotoxin challenge or polymicrobial sepsis and characterized circulating CD71(+) erythroid (CD235a(+)) cells in human neonates. Adoptive transfer or an Ab-mediated reduction in neonatal CD71(+) erythroid splenocytes did not alter murine neonatal survival to endotoxin challenge or polymicrobial sepsis challenge. Ex vivo immunosuppression of stimulated adult CD11b(+) cells was not limited to neonatal splenocytes; it also occurred with adult and neonatal bone marrow. Animals treated with anti-CD71 Ab showed reduced splenic bacterial load following bacterial challenge compared with isotype-treated mice. However, adoptive transfer of enriched CD71(+) erythroid splenocytes to CD71(+)-reduced animals did not reduce bacterial clearance. Human CD71(+) CD235a(+) cells were common among cord blood mononuclear cells and were shown to be reticulocytes. In summary, a lack of effect on murine survival to polymicrobial sepsis following adoptive transfer or diminution of CD71(+) erythroid splenocytes under these experimental conditions suggests that the impact of these cells on neonatal infection risk and progression may be limited. An unanticipated immune priming effect of anti-CD71 Ab treatment, rather than a reduction in immunosuppressive CD71(+) erythroid splenocytes, was likely responsible for the reported enhanced bacterial clearance. In humans, the well-described rapid decrease in circulating reticulocytes after birth suggests that they may have a limited role in reducing inflammation secondary to microbial colonization.
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