Abstract

Neonatal and adult neutrophils are distinctly different from one another due to well-defined and documented deficiencies in neonatal cells, including impaired functions, reduced concentrations of microbicidal proteins and enzymes necessary for pathogen destruction, and variances in cell surface receptors. Neutrophil maturation is clearly demonstrated throughout pregnancy from the earliest hematopoietic precursors in the yolk sac to the well-developed myeloid progenitor cells in the bone marrow around the seventh month of gestation. Notable deficiencies of neonatal neutrophils are generally correlated with gestational age and clinical condition, so that the least functional neutrophils are found in the youngest, sickest neonates. Interruption of normal gestation secondary to preterm birth exposes these shortcomings and places the neonate at an exceptionally high rate of infection and sepsis-related mortality. Because the fetus develops in a sterile environment, neonatal adaptive immune responses are deficient from lack of antigen exposure in utero. Newborns must therefore rely on innate immunity to protect against early infection. Neutrophils are a vital component of innate immunity since they are the first cells to respond to and defend against bacterial, viral, and fungal infections. However, notable phenotypic and functional disparities exist between neonatal and adult cells. Below is review of neutrophil ontogeny, as well as a discussion regarding known differences between preterm and term neonatal and adult neutrophils with respect to cell membrane receptors and functions. Our analysis will also explain how these variations decrease with postnatal age.

Highlights

  • The creation of life through human pregnancy is an astonishing achievement of nature, by which the allogeneic fetus is protected from maternal rejection through placental separation of fetal and maternal vascular systems as well as immunosuppression resulting from high levels of maternal progesterone and placental production of glucocorticoids [1]

  • We explore differences between neonatal and adult neutrophils, describe neutrophil maturation throughout pregnancy, and highlight therapies trialed in neonates to enhance neutrophil function

  • Degranulation capabilities are similar between term neonatal and adult neutrophils, while those from preterm infants have considerable impairments in the release of bactericidal/ permeability-increasing protein (BPI), elastase, and lactoferrin when compared to either term neonatal or adult cells [66, 67]

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Summary

INTRODUCTION

The creation of life through human pregnancy is an astonishing achievement of nature, by which the allogeneic fetus is protected from maternal rejection through placental separation of fetal and maternal vascular systems as well as immunosuppression resulting from high levels of maternal progesterone and placental production of glucocorticoids [1]. Notable phenotypic and functional disparities exist between neonatal and adult cells The severity of these impairments is inversely related to gestational age (GA), revealing progressive neutrophil maturation throughout pregnancy, from the earliest hematopoietic precursors in the yolk sac to the well-developed myeloid progenitor cells in the bone marrow around the seventh month of pregnancy. For more than 50 years, scientists have been striving to understand the intrinsic mechanisms underpinning the normal transition of the suppressed in utero neutrophil into the fully functional postpartum cell capable of combating pathogenic organisms This quest is even more urgent for extremely premature neonates, who are born at the limits of viability, and join the world before the immune developmental program is properly executed. A delicate balance between neutrophil maturation, bone marrow storage and release, intravascular margination, and migration into peripheral tissues is closely regulated by conventional dendritic cells through the controlled production of granulocyte colony-stimulating factor (G-CSF), CXCL1, CCL2, and CXCL10 [27]

Proliferative Bone Marrow Pool
Rolling and firm adhesion
Diminished Neutrophil Production and Neonatal Neutropenia
Neutrophil Pools
Microbicidal Proteins and Activity
Chemotaxis and Migration
Respiratory burst
NEUTROPHILS AND THE MICROBIOME
NEONATAL NEUTROPHILS AND IMMUNOLOGIC QUID PRO QUO
Findings
CONCLUSION
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