The Complement System of the Newborn Infant

Drew, John H.; Arroyave, Carlos M.

doi:10.1159/000241276

Cited by 45 publications

(37 citation statements)

References 3 publications

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“…In the few reports also including studies of complement in low birth weight infants, classical as well as alternative complement activity have generally been found to be lower in low birth weight than in normal term infants (1,6,8,14,16). But it is not clear from these studies whether the defect of complement activity in low birth weight infants is the result of premature birth (6,8) or of intrauterine growth retardation (1,14,16). The purposes of the present study were to compare complement activity of both pathways in AGA and SGA low birth weight newborns, and to determine the influence of birth weight and gestational age on complement development in such infants.…”

Section: Discussionmentioning

confidence: 99%

“…Complement activity is lower in low birth weight infants than in term infants; however, the relationship of gestational age and/ or birth weight to the level of complement activity is still controversial (1,6,8,14,16). The purpose of the present study was to investigate the effects of birth weight and gestational age on complement development (CH50 and kinetics of both CP and AP, C3, and Factor B levels) in low birth weight infants divided into appropriate and small for gestational age groups.…”

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confidence: 99%

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Activity of Classical and Alternative Pathways of Complement in Preterm and Small for Gestational Age Infants

et al. 1984

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SummaryComplement activity was compared in 50 low birth weight infants divided into appropriate and small for gestational age groups; the influence of birth weight and gestational age on complement development was also investigated. CHW and kinetics (tHso) of both classical and alternative pathway activity of complement, C3, and Factor B levels were significantly higher in small for gestational age infants (classical pathway CHs, 630 HU/ml f 184 SD, C P tHs, 77 min + 47; aternative pathway CHS0, 44.8 HU/ml & 11.3; AP tHso, 56 min f 43; C3, 73.98 mg/dl f 12.68; and Factor B, 13.17 mg/dl 2 3.67) than in weight-matched appropriate for gestational age infants (CP CHW, 523 HU/ml 2 152; C P tH9, 105 min + 49; AP CHW, 38.8 HU/ml f 13; AP tHW, 90 min 2 53; C3, 58.14 mg/dl f 9.43; and Factor B, 9.32 mg/dl+ 1.73). Complement values were lower in low birth weight infants than in adult controls ( P < 0.001 in all cases). All complement parameters were mainly correlated with gestational age; CHso values of the classical and alternative pathways were also highly correlated with each other

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Activity of Classical and Alternative Pathways of Complement in Preterm and Small for Gestational Age Infants

et al. 1984

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“…Several studies described reduced amounts of complement factors with weak activity in newborns (26)(27)(28)(29), impairing the clearance of bacterial infections. Similarly, there is a lack of human complement as well as dysfunctional mouse complement in humanized mice (30)(31)(32).…”

Section: Il2rgmentioning

confidence: 99%

Humanized Mice, a New Model To Study the Influence of Drug Treatment on Neonatal Sepsis

et al. 2013

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cBacterial infection with group B Streptococcus (GBS) represents a prominent threat to neonates and fetuses in the Western world, causing severe organ damage and even death. To improve current therapeutic strategies and to investigate new approaches, an appropriate in vivo model to study the immune response of a human immune system is needed. Therefore, we introduced humanized mice as a new model for GBS-induced sepsis. Humanized mice feature deficiencies similar to those found in neonates, such as lower immunoglobulin levels and myeloid cell dysfunction. Due to the husbandry in specific-pathogen-free (SPF) facilities, the human immune cells in these mice also exhibit a naive phenotype which mimics the conditions in fetuses/ neonates. Following infection, cytokine release and leukocyte trafficking from the bone marrow to the lymphoid organ (spleen) and into the peritoneum (site of infection) as well as bacterial spreading and clearance were traceable in the humanized mice. Furthermore, we investigated the effects of betamethasone and indomethacin treatment using this novel sepsis model. Although both drugs are commonly used in perinatal care, little is known about their effects on the neonatal immune system. Treatment of infected humanized mice not only induced the reduction of human leukocytes in the spleen but also increased the bacterial load in all analyzed organs, including the brain, which did not show infiltration of live GBS in untreated controls. These studies demonstrate the utility of the humanized mice as a new model to study an immature human immune response during bacterial infection and allow the investigation of side effects induced by various treatments.

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“…In a preliminary study, sera from three healthy term neonates <24 h of age promoted significant opsonophagocytosis of clinical isolate 515, whereas strain 090 grew in each of these sera. It is possible, however, that the range in physiological deficiency of classical pathway components described for neonatal sera (43,44) has critical functional significance that relates to the pathogenesis of type Ia, group B streptococcal disease in select hosts.…”

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confidence: 99%

Antibody-independent Classical Pathway-mediated Opsonophagocytosis of Type Ia, Group B Streptococcus

Baker¹,

Edwards²,

Webb³

et al. 1982

J. Clin. Invest.

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AB S T R A C T The opsonophagocytic requirements of human sera containing endogenous complement for a variety of type Ia, and group B streptococcal strains were defined. Significant reduction (290%) in colonyforming units was noted after a 40-min incubation for the highly encapsulated, mouse-passed prototype strain 090 by sera containing moderate to high concentrations of antibody to type Ia polysaccharide (mean, 16.5 gg/ml), whereas bacterial growth occurred in 25 sera with low levels of specific antibody (mean, 2.1 ug/ml). This absolute requirement for a critical amount of specific antibody in promoting opsonophagocytic killing of strain 090 was not found when 18 fresh clinical type la isolates were tested. In antibody-deficient and agammaglobulinemic sera, respectively, mean reductions in colony-forming units of 94 and 95% were seen for fresh clinical isolates, whereas strain 090 was not killed by polymorphonuclear leukocytes in the presence of these sera. All strains required a considerable amount of specific antibody for alternative pathwaymediated opsonophagocytosis. That opsonophagocytic killing of clinical type Ia isolates was mediated by the classical pathway in a nonantibody-dependent fashion was shown when MgEGTA chelation of agammaglobulinernic serum or use of serum deficient in C2 resulted in bacterial growth. The addition of C2 to C2-deficient serum restored bactericidal activity of this serum. These experiments indicate that substances other than the exposed surface of the type Ta capsular polysac-

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The Complement System of the Newborn Infant

Cited by 45 publications

References 3 publications

Activity of Classical and Alternative Pathways of Complement in Preterm and Small for Gestational Age Infants

Activity of Classical and Alternative Pathways of Complement in Preterm and Small for Gestational Age Infants

Humanized Mice, a New Model To Study the Influence of Drug Treatment on Neonatal Sepsis

Antibody-independent Classical Pathway-mediated Opsonophagocytosis of Type Ia, Group B Streptococcus

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