Different maturation of neutrophil chemotaxis in term and preterm newborn infants

Sacchi, F; Rondini, G; Mingrat, G.; Stronati, Mauro; Gancia, Gian Paolo; Marseglia, Gian Luigi; Siccardi, Antonio G.

doi:10.1016/s0022-3476(82)80139-x

Cited by 53 publications

(23 citation statements)

References 9 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In most assays, neutrophils from newborn infants migrate at about half the speed travelled by adult cells (Miller, 1971;Klein et al, 1977;Pahwa et al, 1977;Anderson et al, 1981;Boner et al, 1982;Sacchi et al, 1982;Krause et al, 1986a;Carr et al, 1992b;Wolach et al, 1998). Chemotaxis, or cell movement towards an inflammatory stimulus, involves the cell's ability to detect an inflammatory signal, adhere to tissue matrix through adhesion receptors and redistribute those receptors over the cell membrane in order to propel the cell forward while letting go of the surface it is leaving behind.…”

Section: Chemotaxismentioning

confidence: 99%

See 1 more Smart Citation

Neutrophil Production and Function in Newborn Infants

Carr¹

2000

Br J Haematol

192

157

View full text Add to dashboard Cite

Section: Chemotaxismentioning

confidence: 99%

“…The earliest study of postnatal neutrophil maturation compared preterm neonates born before 34 weeks gestation with those born after 34 weeks and with full term deliveries (Sacchi et al, 1982). Term infants had achieved adult chemotactic performance by 2 weeks postnatal age.…”

Section: Chemotaxismentioning

confidence: 99%

Neutrophil Production and Function in Newborn Infants

Carr¹

2000

Br J Haematol

192

157

View full text Add to dashboard Cite

“…Although neonatal PMN are capable of ingesting and killing microorganisms (1,2), chemotaxis of these cells is markedly impaired in vitro and in vivo (3)(4)(5)(6)(7). The mechanism(s) involved in the pathogenesis of abnormal neonatal PMN chemotaxis are unknown.…”

mentioning

confidence: 99%

Defective membrane potential changes in neutrophils from human neonates.

Sacchi¹,

Hill²

1984

The Journal of Experimental Medicine

View full text Add to dashboard Cite

DEFECTIVE MEMBRANE POTENTIAL CHANGES IN NEUTROPHILS FROM HUMAN NEONATESBe FULVIO SACCHI AND HARRY R. HILLA number of studies have been carried out to determine the functional activity of polymorphonuclear leukocytes (PMN) from human neonates in an attempt to explain their unusual susceptibility to infection. Although neonatal PMN are capable of ingesting and killing microorganisms (1, 2), chemotaxis of these cells is markedly impaired in vitro and in vivo (3-7). The mechanism(s) involved in the pathogenesis of abnormal neonatal PMN chemotaxis are unknown. Miller (6) has reported that neonatal PMN have a decreased ability to deform following exposure to chemotactic stimuli, while Anderson and co-workers (7) found that neonatal PMN fail to form uropods and to redistribute adhesion sites. The decreased ability of these cells to change shape and form surface projections suggests that the functional defect may be at the level of the cell membrane. There does not appear to be a significant abnormality in the interaction between chemotactic factor and cell membrane-bound chemotactic factor receptors on resting neonatal PMN at 37°C (7,8). The defect may be, therefore, at a level beyond this initial interaction.The recent introduction of spectrofluorometric techniques for measuring critical ionic changes at the membrane and in the intracellular milieu has led to a better understanding of the events associated with phagocyte activation (9-14). Such probes include the cyanine dye 3-3 dipentyloxacarbocyanine [DiOCs(3)], which is sensitive to changes in membrane potential (11,12,15), and Quin 2/AM (13, 16), which assesses changes in intracellular free calcium. We have used these two fluorescent probes to assess the cellular events following chemotactic factor-receptor interaction in PMN from human neonates and compared the results with those obtained in PMN from adults. Materials and Methods PMN Preparations.Whole blood was obtained from peripheral veins of healthy adults and from the umbilical cords of normal-term neonates in acid citrate dextrose (Becton Dickinson and Co., Rutherford, N J). The blood was allowed to settle in 1% dextran (Pharmacia, Piscataway, N J) and the PMN were separated on Ficoil-Hypaque (Pharmacia) gradients. Contaminating erythrocytes were hypotonicaily lysed, and the PMN suspensions (98%) were washed in phosphate-buffered saline (PBS, pH 7.4) and suspended in a modified Hanks' balanced salt solution (HBSS) containing 124 mM NaCI, 4 mM KCI, 0.64 mM NaH~PO4, 0.66 mM K2HPO4, 15.2 mM NaHCOs, 10 mM Hepes buffer, 5.56 mM glucose, and 1.6 mM CaCI2 or 2 mM EGTA. The pH was adjusted to 7.4.

show abstract

“…For instance, a n important problem in neonatology practice involves the very high incidence of nosocomial infections in extremely preterm infants (18). The basis for this defective antibacterial defense appears to involve a relatively small neutrophil reserve per kilogram of body weight (19,20), a significant limitation in up-regulating neutrophil production during bacterial infection (2 I), and relatively poor neutrophil adherence, chemotaxis, and superoxide generation (22)(23)(24)(25)(26)(27). Effective and safe methods of improving neutrophil production and function in preterm neonates would be of interest as potential means of decreasing the incidence or severity of infections.…”

Section: Resultsmentioning

confidence: 99%