The role of specific antibody in alternative complement pathway-mediated opsonophagocytosis of type III, group B Streptococcus.

Edwards, Morven S.; Nicholson‐Weller, Anne; Baker, Carol J.; Kasper, Dennis L.

doi:10.1084/jem.151.5.1275

Cited by 185 publications

(123 citation statements)

References 38 publications

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“…Low concentrations of Ab to most mastitis pathogens are usually found in milk, but it is not known if Ab may be a limiting factor for complementdependent bactericidal activity. In most cases, the activation of the complement in the presence of Ab is by CP, but rather high concentrations of Ab can also induce the deposition of C3 on bacteria through AP, for example on type III S. agalactiae [25], or on certain strains of mastitis isolates of E. coli [44]. Depending on the strain, the complement alone was sufficient or the complement plus Ab were necessary to kill serum-sensitive E. coli [44].…”

Section: Bactericidal and Hemolytic Activities In Normal Milkmentioning

confidence: 99%

The complement in milk and defense of the bovine mammary gland against infections

Rainard

2003

Vet. Res.

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-The mammary gland of dairy cows, which is prone to infection by various bacteria, mobilizes local and systemic immune defenses to cope with pathogens. The complement system plays an important part in the innate immunity against microorganisms through its bactericidal, opsonic, and phlogistic functions. The amount of the complement in the milk of healthy glands of dairy cows is low. Moreover, the classical pathway of activation is not functional because of a shortage in C1q. By contrast, the alternative pathway is active, deposits C3b and C3bi on bacteria, and generates amounts of C5a which are highly variable among cows. A slight inhibition of the bactericidal/hemolytic activities, of the deposition of C1q on bacteria, and of the phlogistic activity of C5a makes milk a rather anti-inflammatory fluid. The inhibitory activity does not involve C3b/ C3bi deposition on bacteria, nor the generation of C5a by the alternative pathway. When inflammation develops, the blood-derived complement components overcome the inhibitions and complement-dependent bactericidal, opsonic and phlogistic activities may be high in milk. Further research is necessary to evaluate the contribution of C5a to the recruitment of leukocytes in the mammary gland, and to specify the links between the complement system and the response of resident cells (leukocytes and mammary epithelial cells) to infection stimulus. This will help to define the contribution of the complement system to resistance against mastitis, and could help to differentiate animals more or less resistant to this frequent and costly disease.

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Section: Bactericidal and Hemolytic Activities In Normal Milkmentioning

confidence: 99%

The complement in milk and defense of the bovine mammary gland against infections

Rainard

2003

Vet. Res.

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“…The developing reagent consisted of 0.4 mg/mL of o-phenylenediamine in 0.2 M Na2HP04 (pH 5.0 with 0.1 M citric acid), containing 0. 4 Biochemical assay for reactivity of C3 thiolester bond. Nucleophilic amines, such as CH3NH2, are inherently reactive with thiolester bonds; binding of the nucleophile is stoichiometric, with I mol of the nucleophile covalently bound for each mol of thiolester disrupted (20).…”

Section: Methodsmentioning

confidence: 99%

“…This predisposition to infection is ascribable, at least in part, to age-related defects in host defense (2, 3). Primary among humoral defenses are the complement proteins, which serve as opsonins for common neonatal pathogens such as the group B Streptococcus or the K1 capsular serotype of Escherichia coli (4,5). …”

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confidence: 99%

Biochemical Abnormalities of the Third Component of Complement in Neonates

Zach

Hostetter

1989

Pediatr Res

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ABSTRACT. The third component of complement, C3, is of central importance as an opsonin in the nonimmune host. Although gestational deficiencies in C3 levels are well recognized in neonates, defects in complement-mediated functions have not in every case correlated with low levels of complement proteins. Because opsonic functions of C3 are mediated through a reactive thiolester bond, we hypothesized that a biochemical dysfunction at this active site could explain the newborn's predisposition to infection, even with relatively normal C3 levels. We therefore examined the biochemical integrity of the C3 thiolester in an assay independent of all other complement proteins. As measured by ELISA, mean C3 levels from 44 neonates (24-43 wk) were significantly lower in infants < 30 wk gestational age (0.79 f 0.13 mg/mL) than in full-term newborns (1.19 +1 0.27 mg/ml, p < 0.05). Furthermore, biochemical reactivity of the thiolester bond, as measured by incorporation of the radiolabeled nucleophile, methylamine, correlated significantly with gestational age ( r = 0.45, p < 0.01). Functional C3 was defined as the product of thiolester reactivity and C3 level; 9/11 premature and 2/ 17 full-term infants had levels of functional C3 which were less than 50% of the adult norm. Structural analysis of neonatal C3 revealed the two-chain structure in all neonates; four neonates had an additional band at 205 kD which may represent an impairment in posttranslational processing of a precursor molecule. We conclude that defects in thiolester reactivity may constitute a newly identified mechanism for the newborn's susceptibility to infection. (Pediatr Res 26: 116-120, 1989) Abbreviations PAS, pooled adult serum CH3NH2, methylamine Sepsis is a leading cause of morbidity and mortality in neonates, with premature infants affected more frequently than fullterm newborns (I). This predisposition to infection is ascribable, at least in part, to age-related defects in host defense (2, 3). Primary among humoral defenses are the complement proteins, which serve as opsonins for common neonatal pathogens such as the group B Streptococcus or the K1 capsular serotype of Escherichia coli (4,5).

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“…The importance of PMNs and specific Ab in host defense against III GBS is well recognized. [1][2][3] Neutropenia is a clinical feature of GBS sepsis that has been associated with poor outcome. 36 Cairo et al 37,38 investigated the potential role of leukocyte transfusions to treat infants with neonatal sepsis.…”

Section: Discussionmentioning

confidence: 99%

“…However, previous studies suggest that these components of host defense are deficient in the neonate. 2,3 Furthermore, there are qualitative and quantitative deficiencies in PMN function in neonates. 4 -6 Cytokines, such as tumor necrosis factor-␣ (TNF-␣), granulocyte colony-stimulating factor (G-CSF), and granulocyte-macrophage colony-stimulating factor (GM-CSF), augment the bactericidal activity of PMNs from adults against Staphylococcus aureus, nontypable Hemophilus influenzae, Legionella pneumophila, and Candida albicans.…”

mentioning

confidence: 99%