Supplemental Complement Component C9 Enhances the Capacity of Neonatal Serum to Kill Multiple Isolates of Pathogenic Escherichia coli

Lassiter, Herbert A.; Wilson, J. L.; Feldhoff, Richard C.; Hoffpauir, John; Klueber, Kathleen M.

doi:10.1203/00006450-199404000-00002

Cited by 29 publications

(4 citation statements)

References 12 publications

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“…The defective activation of C3 could contribute to the increased susceptibility of neonates to certain bacterial infection. Lassiter et al (1992Lassiter et al ( ,1994 confirmed the importance of very low C9 concentration in term neonatal sera to diminished capacity to kill E. coli, since it was vastly improved through the addition of purified C9 alone. Since multiple units of C9 are recruited in formation of the final lytic pore of the terminal complement pathway, Lassiter's group also showed that C9 supplementation of neonatal serum under subbactericidal conditions greatly increased the delivery of antibiotics leading to increased anti-microbial efficacy (Jung et al 1998).…”

Section: Response Of Neonatal Complement To Bacteriasupporting

confidence: 54%

Off to a slow start: Under-development of the complement system in term newborns is more substantial following premature birth

2012

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Section: Response Of Neonatal Complement To Bacteriasupporting

confidence: 54%

Off to a slow start: Under-development of the complement system in term newborns is more substantial following premature birth

2012

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“…In addition, Lassiter et al. 31,35 demonstrated that deficiency of C9 component is associated with diminished deposition of C9 on E. coli and killing of the bacteria in neonatal rats. In AB, OmpA – E. coli could not survive at any inoculum size, whereas it survived efficiently at 10 6 CFU/ml in CB.…”

Section: Discussionmentioning

confidence: 99%

“…The C9 deficiency of cord serum is in agreement with several previous studies in which the investigators have shown that neonatal serum is significantly deficient in C9 (260 + 50 lg/ml in adults versus < 42 lg/ml in neonates, 30 ). In addition, Lassiter et al 31,35 demonstrated that deficiency of C9 component is associated with diminished deposition of C9 on E. coli and killing of the bacteria in neonatal rats. In AB, OmpA -E. coli could not survive at any inoculum size, whereas it survived efficiently at 10 6 CFU/ml in CB.…”

Section: Discussionmentioning

confidence: 99%

Effects of complement regulators bound to Escherichia coli K1 and Group B Streptococcus on the interaction with host cells

2008

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Summary Escherichia coli K1 and Group B Streptococcus (GBS) are the most common bacteria that cause meningitis during the neonatal period. Complement, the first line of defence in the host, acts on these bacteria to opsonize with various components of complement for subsequent presentation to phagocytes. To counteract these opsonization effects, E. coli and GBS bind to the complement regulators C4 binding protein and Factor H, respectively. Nonetheless, the deposition of complement components on these two bacteria from neonatal serum and their effect on the host cell interaction is unclear. Here we demonstrated that the deposition of complement proteins from adult serum prevented the invasion of E. coli into human brain microvascular endothelial cells, whereas the invasion of GBS was enhanced. In contrast, treatment with cord serum had no effect on the invasion of both these bacteria. We also examined the effect of the deposited complement proteins on phagocytosis using THP‐1 cells and THP‐1 cells differentiated into macrophages. Escherichia coli treated with adult serum neither attached nor entered these cells, whereas GBS was phagocytosed and survived efficiently. We further demonstrate that the inhibitory effect of complement proteins is the result of the bound complement inhibitors C4b‐binding protein, in the case of E. coli, and Factor H, in the case of GBS. Taken together, these results suggest that E. coli and GBS utilize contrasting mechanisms of complement‐mediated interactions with their target cells for successful establishment of disease.

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“…It is recognized that neonates are deficient in C9 and are highly susceptible to E. coli sepsis. Supplementation of C9 to neonatal serum enhances the capacity of neonatal serum to kill E. coli [30]. Hence, the association of low C9 with septic shock in GNB patients is plausible in this regard, with low levels likely reflecting over-consumption of this key complement protein.…”

Section: Discussionmentioning

confidence: 99%

Complement levels in patients with bloodstream infection due to Staphylococcus aureus or Gram-negative bacteria

Eichenberger

Dagher

Ruffin

et al. 2020

Eur J Clin Microbiol Infect Dis

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The complement system is a vital component of the innate immune system, though its role in bacteremia is poorly understood. We present complement levels in Staphylococcus aureus bacteremia (SAB) and Gram-negative bacteremia (GNB) and describe observed associations of complement levels with clinical outcomes. Complement and cytokine levels were measured in serum samples from 20 hospitalized patients with SAB, 20 hospitalized patients with GNB, 10 non-infected hospitalized patients, and 10 community controls. C5a levels were significantly higher in patients with SAB as compared to patients with GNB. Low C4 and C3 levels were associated with septic shock and 30-day mortality in patients with GNB, and elevated C3 was associated with a desirable outcome defined as absence of (1) septic shock, (2) acute renal failure, and (3) death within 30 days of bacteremia. Low levels of C9 were associated with septic shock in patients with GNB but not SAB. Elevated IL-10 was associated with increased 30-day mortality in patients with SAB. Complement profiles differ in patients with SAB and those with GNB. Measurement of IL-10 in patients with SAB and of C4, C3, and C9 in patients with GNB may help to identify those at higher risk for poor outcomes.

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Supplemental Complement Component C9 Enhances the Capacity of Neonatal Serum to Kill Multiple Isolates of Pathogenic Escherichia coli

Cited by 29 publications

References 12 publications

Off to a slow start: Under-development of the complement system in term newborns is more substantial following premature birth

Off to a slow start: Under-development of the complement system in term newborns is more substantial following premature birth

Effects of complement regulators bound to Escherichia coli K1 and Group B Streptococcus on the interaction with host cells

Complement levels in patients with bloodstream infection due to Staphylococcus aureus or Gram-negative bacteria

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