Influence of different immunoglobulin G preparations on phagocytosis of pseudomonas aeruginosa by polymorphonuclear granulocytes

Trautmann, Matthias; Triest, Konstanze; Hofstaetter, T.; Seiler, F. R.; Hahn, Helmut

doi:10.1016/s0176-6724(85)80012-2

Cited by 6 publications

(6 citation statements)

References 14 publications

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“…We found that F(ab′) 2 ≫ Fab at promoting complement-dependent opsonophagocytic killing of S. pneumoniae and lysis of H. influenzae , and have attributed this difference to the ability of F(ab′) 2 to agglutinate and, therefore, increase the size of bacterial targets. This effect is likely not specific to these two microbes, since opsonophagocytic killing of Pseudomonas aeruginosa is also enhanced by F(ab′) 2 but not Fab, and importantly, this required the presence of active complement (Trautmann et al, 1985). Additionally, others have shown that F(ab′) 2 could promote clearance of invasive bacterial infection while Fab could not, suggesting that agglutination may play a role independent of Fc-effector function in vivo as well (Ax et al, 1981).…”

Section: Discussionmentioning

confidence: 99%

“…Some studies show that both fragments promote alternative pathway-dependent effects equally, while others show that show that F(ab′) 2 is better than Fab at activating the complement system (Ax et al, 1981; Ehrnst, 1978; Moore et al, 1982; Trautmann et al, 1985; Winkelstein and Shin, 1974). Without Fc, it is unlikely that either molecule directly activates the complement cascade by binding C1q.…”

Section: Discussionmentioning

confidence: 99%

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Minimization of Bacterial Size Allows for Complement Evasion and Is Overcome by the Agglutinating Effect of Antibody

Dalia

Weiser

2011

Cell Host & Microbe

118

122

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SUMMARY The complement system, which functions by lysing pathogens directly or by promoting their uptake by phagocytes, is critical for controlling many microbial infections. Here we show that in Streptococcus pneumoniae, increasing bacterial chain length sensitizes this pathogen to complement deposition and subsequent uptake by human neutrophils. Consistent with this, we show that minimizing chain length provides wild-type bacteria with a competitive advantage in vivo in a model of systemic infection. Investigating how the host overcomes this virulence strategy, we find that antibody promotes complement-dependent opsonophagocytic killing of Streptococcus pneumoniae and lysis of Haemophilus influenzae independent of Fc-mediated effector functions. Consistent with the agglutinating effect of antibody, F(ab′)2 but not Fab could promote this effect. Therefore, increasing pathogen size, whether by natural changes in cellular morphology or via antibody-mediated agglutination, promotes complement-dependent killing. These observations have broad implications for how cell size and morphology can affect virulence among pathogenic microbes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Minimization of Bacterial Size Allows for Complement Evasion and Is Overcome by the Agglutinating Effect of Antibody

Dalia

Weiser

2011

Cell Host & Microbe

118

122

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“…Even though Fab fragments that also lack Fc bind equally compared to F(ab′) 2 , these are monovalent and consequently do not agglutinate their target or promote complement activation or killing. This effect of F(ab′) 2 , but not Fab, has been shown for H. influenzae , for which activation of the complement cascade results in direct lysis, and for S. pneumoniae and Pseudomonas aeruginosa where complement deposition causes opsonization and uptake by phagocytes(8, 28). In this manner, agglutinating antibody is able to subvert virulence factors such as capsular polysaccharide that otherwise limit complement deposition on the cell surface.…”

Section: The Host Fights Backmentioning

confidence: 70%

The battle with the host over microbial size

Weiser

2013

Current Opinion in Microbiology

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An eponymous feature of microbes is their small size, and size affects their pathogenesis. The recognition of microbes by host factors, for example, is often dependent on the density and number of molecular interactions occurring over a limited surface area. As a consequence, certain antimicrobial substances, such as complement, appear to target particles with a larger surface area more effectively. Although microbes may inhibit these antimicrobial activities by minimizing their effective size, the host uses defenses such as agglutination by immunoglobulin to counteract this microbial evasion strategy. Some successful pathogens in turn are able to prevent immune mediated clearance by expressing virulence factors that block agglutination. Thus, microbial size is one of the battlegrounds between microbial survival and host defense.

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“…Our results using F(ab′) 2 fragments do not distinguish between these two possibilities, as these fragments themselves can promote activation of the alternative complement pathway [37–39]. We also examined the effect of Fab fragments, as classically these have been thought to be unable to promote complement activation and opsonization [40]. Using this assumption, our results demonstrating promotion of bacterial adherence by Fab fragments in the presence of NHS would suggest that these fragments are directly binding to sites on the bacterial surface that intrinsically interfere with complement activation.…”

Section: Discussionmentioning

confidence: 85%

Specific antibody promotes opsonization and PMN-mediated killing of phagocytosis-resistantEnterococcus faecium

Rakita¹,

Quan²,

Jacques-Palaz³

et al. 2000

FEMS Immunology &Amp; Medical Microbiology

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Many clinical isolates of Enterococcus faecium are resistant to neutrophil (PMN)-mediated phagocytosis and killing in the presence of normal human serum. We have now examined the ability of specific polyclonal rabbit antibodies to promote opsonization and killing of phagocytosis-resistant E. faecium. Immune rabbit serum generated against formalin-killed E. faecium TX0016, a phagocytosis-resistant strain, markedly promoted binding of TX0016 organisms to PMNs and PMN-mediated killing. These effects were dramatically reduced by (a) adsorption of immune serum with E. faecium TX0016, but not by adsorption with a strain of E. faecium susceptible to phagocytosis, and (b) incubation of immune serum with carbohydrate purified from TX0016, but not by incubation with a surface protein extract from TX0016. IgG purified from immune serum was unable by itself to promote bacterial binding to PMNs. However, specific IgG was able to promote binding to PMNs and PMN-mediated killing in the presence of normal human serum as a complement source, as were F(ab')(2) and Fab fragments produced from it, and the alternative pathway of complement was sufficient to promote IgG- and F(ab')(2)-mediated opsonization. PMN complement receptor type 3, but not complement receptor type 1, was involved in bacterial binding to PMNs induced by the combination of F(ab')(2) fragments and normal human serum. These results suggest that opsonization by antibodies potentially directed against bacterial carbohydrate, in conjunction with complement activation, has an important role in the host defense against phagocytosis-resistant E. faecium.

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Influence of different immunoglobulin G preparations on phagocytosis of pseudomonas aeruginosa by polymorphonuclear granulocytes

Cited by 6 publications

References 14 publications

Minimization of Bacterial Size Allows for Complement Evasion and Is Overcome by the Agglutinating Effect of Antibody

Minimization of Bacterial Size Allows for Complement Evasion and Is Overcome by the Agglutinating Effect of Antibody

The battle with the host over microbial size

Specific antibody promotes opsonization and PMN-mediated killing of phagocytosis-resistantEnterococcus faecium

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