Immunology of Staphylococci

Verhoef, J.; Peterson, Phillip K.; Quie, Paul G.

doi:10.1007/978-1-4684-1009-9_4

Cited by 5 publications

(2 citation statements)

References 138 publications

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“…For other encapsulated bacteria, however, the classical pathway does not appear to be required for deposition of opsonic C3b in the presence of specific antibody. Evidence has been presented to support alternative pathway activation in opsonization by specific antibodies of Staphylococcus aureus (35), Bacteroides fragilis (36), and GBS (11). For type III GBS, inhibition of alternative pathway activation can be overcome by specific antibodies, resulting in deposition of C3b on the bacterial surface and opsonophagocytosis by neutrophils (11,25,29).…”

Section: Discussionmentioning

confidence: 99%

Studies of group B streptococcal infection in mice deficient in complement component C3 or C4 demonstrate an essential role for complement in both innate and acquired immunity.

Wessels

Butko²,

Ma³

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

454

334

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Group B streptococci (GBS) cause sepsis and meningitis in neonates and serious infections in adults with underlying chronic illnesses. Specific antibodies have been shown to be an important factor in protective immunity for neonates, but the role of serum complement is less well defined. To elucidate the function of the complement system in immunity to this pathogen, we have used the approach of gene targeting in embryonic stem cells to generate mice totally deficient in complement component C3. Comparison of C3-deficient mice with mice deficient in complement component C4 demonstrated that the 50% lethal dose for GBS infection was reduced by "50-fold and 25-fold, respectively, compared to control mice. GBS were effectively killed in vitro by human blood leukocytes in the presence of specific antibody and C4-deficient serum but not C3-deficient serum. The defective opsonization by C3-deficient serum in vitro was corroborated by in vivo studies in which passive immunization of pregnant dams with specific antibodies conferred protection from GBS challenge to normal and C4-deficient pups but not C3-deficient pups. These results indicate that the alternative pathway is sufficient to mediate effective opsonophagocytosis and protective immunity to GBS in the presence of specific antibody. In contrast, the increased susceptibility to infection of nonimmune mice deficient in either C3 or C4 implies that the classical pathway plays an essential role in host defense against GBS infection in the absence of specific immunity.

show abstract

Section: Discussionmentioning

confidence: 99%

Studies of group B streptococcal infection in mice deficient in complement component C3 or C4 demonstrate an essential role for complement in both innate and acquired immunity.

Wessels

Butko²,

Ma³

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

454

334

View full text Add to dashboard Cite

show abstract

“…The opsonic activity of complement resides in a fragment of its third component, called C3b, and is generated from native C3 by enzymatic cleavage (42). In the absence of complement, staphylococci become opsonized only in immune sera containing high levels of specific antibody (19,32,46,50,55 ity from normal and immune human sera, and from hyperimmune sera raised in rabbits (13,16,38). In addition, 92 peptidoglycan-specific antibody isolated from rabbit immune sera has been shown to exert a direct opsonic effect (16,48 (54) demonstrated that encapsulation of S. aureus interfered with bacterial opsonization in normal human serum.…”

Section: Tank Frfmentioning

confidence: 99%

Phagocytosis and destruction ofStaphylococcus aureus

1981

Veterinary Quarterly

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SUMMARYA review is presented of the phagocytosis and intracellular killing of Staphylococcus aureus by polymorphonuclear and mononuclear leukocytes. Recruitment of adequate numbers of leukocytes to the site of infection occurs through the process of chemotaxis. Recognition of invading staphylococci by the phagocytic cells is mediated through bacterial opsonization. Both processess depend upon the activation of the heat-labile complement system which generates the majority of chemotactic (C5a) and opsonic (C3b) moleculesfor S. aureus phagocytosis. The key role of peptidoglycan in the cell wall of staphylococci in these events is stressed. Attachment and ingestion of opsonized staphylococci occurs via poorly-defined receptors for opsonins in the membrane of the leukocyte. The greater phagocytic capacity of neutrophils as compared to monocytes is not reflected in differences in their membrane receptors for staphylococcal opsonins. Once ingested, staphylococci are rapidly destroyed by oxygen-dependent and oxygen-independent bactericidal mechanisms of the phagocytes. Small numbers of S. aureus may survive within the leukocyte. Special attention is focused on the numerous ways S. aureus is able to hinder, evade, and directly damage the phagocytic defense mechanisms of the host.

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New aspects of staphylococcal infections: emergence of coagulase-negative staphylococci as pathogens

Fleer

Verhoef

1984

Antonie van Leeuwenhoek

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In contrast to the well-established pathogen Staphylococcus aureus, the coagulase-negative staphylococci, formerly collectively called S. epidermidis, were until recently regarded as harmless commensals. During the last two decades, however, the coagulase-negative staphylococci have clearly emerged as pathogens in patients carrying artificial devices, such as prosthetic heart valves, hip prostheses and cerebrospinal fluid shunts, and in patients with compromised host defenses such as premature neonates and cancer and transplant patients. The present paper reviews current insights on classification, bacteriology, pathogenic potential and virulence factors of coagulase-negative staphylococci. In addition, the role of host defense factors in resistance to staphylococcal infection is summarized as well as the main features of the clinical syndromes in which coagulase-negative staphylococci are involved.

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Immunology of Staphylococci

Cited by 5 publications

References 138 publications

Studies of group B streptococcal infection in mice deficient in complement component C3 or C4 demonstrate an essential role for complement in both innate and acquired immunity.

Studies of group B streptococcal infection in mice deficient in complement component C3 or C4 demonstrate an essential role for complement in both innate and acquired immunity.

Phagocytosis and destruction ofStaphylococcus aureus

New aspects of staphylococcal infections: emergence of coagulase-negative staphylococci as pathogens

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