Year: 2002
Type: dissertation
Abstract: Background: Newborn infants are particularly susceptible to bacterial infections due to their immature immune functions.Diagnosis of bacterial infection is difficult because newborn infants present with unspecific clinical symptoms and because of the lack of reliable laboratory markers.In newborn infants, sepsis is the most common cause of systemic inflammation, which is characterized by activation of inflammatory cells, the coagulation system, and the complement system within the circulation.Signs of systemic and pulmonary inflammation are present also in preterm infants with respiratory distress syndrome (RDS).In the newborn infant, the immaturities of the host defence comprise qualitative and quantitative deficiencies of the innate and acquired immunity.Of the innate immune system, polymorphonuclear leukocytes (PMN), important cellular effectors that provide the major host defence against bacterial invasion, have been reported to function suboptimally.Objectives: To study neutrophil CD11b and IL-8 as markers of systemic inflammation and sepsis in newborn infants with early onset sepsis, neutrophil CD11b expression as a marker of systemic inflammation in preterm infants with RDS, and the effects of dexamethasone on phagocyte activation in preterm infants with RDS.In addition, to study the ability of newborn PMNs to release granule contents.Subjects: Newborn infants born at or near term with suspected sepsis (N=35).Healthy term infants ( N=17).Preterm infants with (N=59) and without RDS (N=12).Cord blood samples from preterm (N=21) and term infants (N=30) were obtained for in vitro-stimulation assays.The entire project comprised 174 newborn infants.From 51 of these infants, only cord blood was obtained (preterm 21, term 30).The other 123 were preterm infants with RDS (N=59), healthy preterm infants without RDS (N=12), infants over 29 gestational weeks with suspected earlyonset infection (N=35), and healthy term infants aged 2 to 5 days (N=17).Of the preterm and term infants with only cord blood samples available, 11 (preterm) and 29 (term) were included in two series (I, III).In Study I, 25, and in Study III, 15 healthy adults taking no medication, and with no clinical signs of infection, served as controls.Main results: Neutrophil CD11b expression and plasma IL-8 concentration were higher in septic infants at the initial evaluation.Their sensitivity and specificity with the chosen cut-off value were high.In preterm infants with RDS, neutrophil CD11b expression was increased on the first day of life.The administration of dexamethasone inhibited phagocyte activation and systemic inflammation in preterm infants with RDS.Both preterm and term infants had a lower capacity to increase neutrophil CD11b expression upon in-vitro stimulation, whereas the ability to release BPI was lower only in preterm infants.Conclusions: Neutrophil CD11b expression and plasma IL-8 serve as reliable markers for early onset sepsis in newborn infants born at or near term.In preterm infants, phagocyte activation and systemic inflammation play a role in the pathogenesis of RDS.Because inflammatory factors are important in the etiology of bronchopulmonary dysplasia (BPD), decreased phagocyte activation in the circulation may lead to attenuated pulmonary inflammation and to a reduced severity of BPD.The lower ability of PMN in newborn infants to release granule contents may, at least in part, explain the higher susceptibility of newborn infants to infections than adults.
Source: Työväentutkimus Vuosikirja
Author: Irmeli Nupponen
Language: English
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W1910336980