What is the role of cellular immunity in the pathophysiology of neonatal sepsis?

Updated: Jun 13, 2019
  • Author: Nathan S Gollehon, MD, FAAP; Chief Editor: Muhammad Aslam, MD  more...
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Answer

PMNs are vital for effective killing of bacteria. However, neonatal PMNs are deficient in chemotaxis and killing capacity. Decreased adherence to the endothelial lining of blood vessels reduces their ability to marginate and leave the intravascular space to migrate into the tissues. Once in the tissues, they may fail to degranulate in response to chemotactic factors.

Furthermore, neonatal PMNs are less deformable and thus are less able to move through the extracellular matrix of tissues to reach the site of inflammation and infection. The limited capacity of neonatal PMNs for phagocytosis and killing of bacteria is further impaired when the infant is clinically ill. Finally, neutrophil reserves are easily depleted because of the diminished response of the bone marrow, especially in the premature infant. [12]

Neonatal monocyte concentrations are at adult levels; however, macrophage chemotaxis is impaired and continues to exhibit decreased function into early childhood. The absolute numbers of macrophages are decreased in the lungs and are likely decreased in the liver and spleen as well. The chemotactic and bactericidal activity and the antigen presentation by these cells are also not fully competent at birth. Cytokine production by macrophages is decreased, which may be associated with a corresponding decrease in T-cell production. [13]

Although T cells are found in early gestation in fetal circulation and increase in number from birth to about age 6 months, these cells represent an immature population. These naive cells do not proliferate as readily as adult T cells do when activated, and they do not effectively produce the cytokines that assist with B-cell stimulation and differentiation and granulocyte/monocyte proliferation.

Formation of antigen-specific memory function after primary infection is delayed, and the cytotoxic function of neonatal T cells is 50%-100% as effective as that of adult T cells. At birth, neonates are deficient in memory T cells. As the neonate is exposed to antigenic stimuli, the number of these memory T cells increases.

Natural killer (NK) cells are found in small numbers in the peripheral blood of neonates. These cells are also functionally immature in that they produce far lower levels of interferon gamma (IFN-γ) upon primary stimulation than adult NK cells do. This combination of findings may contribute to the severity of HSV infections in the neonatal period.


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