Opsonin-independent phagocytosis of group B streptococci: role of complement receptor type three

Antal, József; Cunningham, J V; Goodrum, K J

doi:10.1128/iai.60.3.1114-1121.1992

Cited by 39 publications

(26 citation statements)

References 43 publications

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“…These results may have direct relevance to the observation that OKM1 was shown to inhibit the binding of opsonized M. tuberculosis to MDMs to a greater extent than that shown by Leu-15 (44 to 50% versus 34 to 39%, respectively) (44), which strongly suggests that a significant component of the binding of M. tuberculosis to CR3 is opsonin independent, irrespective of the presence or absence of C3 on the bacterial surface. This interpretation par-allels the conclusions reached for the opsonin independence of the binding of zymosan particles to neutrophil CR3 (40) or group B streptococci to CR3 on neutrophils and monocytes (1), where in both cases binding was not inhibited by a large excess of Fab anti-C3.…”

Section: Discussionsupporting

confidence: 81%

“…Stokes et al (48) observed considerable variations among different M. tuberculosis complex strains and other mycobacterial species in the extent of nonopsonic binding to murine macrophages. Similarly, Antal et al (1) noted that the C3-independent binding of another gram-positive bacterium, group B streptococcus, to CR3 is likely strain dependent. The reported studies on M. tuberculosis binding to monocyte/macrophage complement receptors were performed predominantly with the Erdman strain (43,44) or the H37Ra strain (20) grown in rich medium (7H9 broth).…”

Section: Discussionmentioning

confidence: 96%

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Nonopsonic binding of Mycobacterium tuberculosis to human complement receptor type 3 expressed in Chinese hamster ovary cells

et al. 1996

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Nonopsonic invasion of mononuclear phagocytes byMycobacterium tuberculosis is likely important in the establishment of a primary infection in the lung. M. tuberculosis binds to a variety of phagocyte receptors, of which the mannose receptor and complement receptor type 3 (CR3) may support nonopsonic binding. CR3, a ␤ 2 integrin, is a target for diverse intracellular pathogens, but its role in nonopsonic binding remains uncertain. We have examined the binding of M. tuberculosis H37Rv to human CR3 heterologously expressed in Chinese hamster ovary (CHO) cells, thereby circumventing the problems of competing receptors and endogenously synthesized complement, which are inherent in studies with mononuclear phagocytes. The surface expression of CD11b and CD18 was assessed by immunofluorescence, immunobead binding, flow cytometry, and immunoprecipitation with anti-CD11b and anti-CD18 monoclonal antibodies (MAbs). The functional activity of the surface-expressed CD11b/CD18 (CR3) heterodimer was confirmed by rosetting with C3bi-coated microspheres. We found that M. tuberculosis bound four-to fivefold more avidly to CR3-expressing CHO cells than to wild-type cells and, importantly, that this binding was at similar levels in the presence of fresh or heat-inactivated human or bovine serum or no serum. In contrast, Mycobacterium smegmatis bound poorly to CR3-expressing CHO cells in the absence of serum, but after opsonization in serum, binding was comparable to that of M. tuberculosis. The binding of M. tuberculosis to the transfected CHO cells was CR3 specific, as it was inhibited by anti-CR3 MAbs, particularly the anti-CD11b MAbs LM2/1 (I domain epitope) and OKM1 (C-terminal epitope), neither of which inhibit C3bi binding. MAb 2LPM19c, which recognizes the C3bi-binding site on CD11b, had little or no effect on M. tuberculosis binding. The converse was found for the binding of opsonized M. smegmatis, which was strongly inhibited by 2LPM19c but unaffected by LM2/1 or OKM1. CR3-specific binding was also evidenced by the failure of M. tuberculosis to bind to CHO cells transfected with an irrelevant surface protein (angiotensin-converting enzyme) in the presence or absence of serum. We conclude that the binding of M. tuberculosis H37Rv to CR3 expressed in CHO cells is predominantly nonopsonic and that the organism likely expresses a ligand that binds directly to CR3.on July 6, 2020 by guest http://iai.asm.org/ Downloaded from MATERIALS AND METHODS Bacteria. M. tuberculosis H37Rv (ATCC 27294) and Mycobacterium smegmatis (ATCC 19420) were maintained on Lowenstein-Jensen slopes. Bacterial stocks required for the in vitro infection assays were generated as follows. The confluent growth of M. tuberculosis on a Lowenstein-Jensen slope was dislodged and suspended in 8 ml of Kirchner's medium, agitated to break up the larger clumps, and allowed to settle for 10 min at room temperature. The top 5 ml was used to inoculate 100 ml of Kirchner's medium and grown with shaking (200 rpm) at 37ЊC for 2 weeks. Fifty milliliters of the 2-week-old c...

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Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 96%

Nonopsonic binding of Mycobacterium tuberculosis to human complement receptor type 3 expressed in Chinese hamster ovary cells

et al. 1996

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“…In vitro and in vivo virulence assays with unencapsulated or asialo mutants support the hypothesis that type III capsule serves as a virulence factor [11,12]. Other studies have shown that well encapsulated GBS are able to enter and persist in macrophages by evading intracellular opsonin-mediated antibacterial activities [13,14]. The role of the polysaccharidic capsule in the opsoninindependent uptake is so far unknown.…”

Section: Introductionmentioning

confidence: 59%

Streptococcus suis and group B Streptococcus differ in their interactions with murine macrophages

Segura¹

1998

FEMS Immunology and Medical Microbiology

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Streptococcus suis type 2 and group B Streptococcus type III (GBS) are important encapsulated bacterial species causing meningitis. In the present study we compared quantitatively the uptake and intracellular survival of S. suis type 2 and GBS type III with murine macrophages in non-opsonic conditions. The role of the capsule of both pathogens was also studied using previously obtained unencapsulated isogenic mutants. Encapsulated S. suis wild-type strain was practically not phagocytosed, while the unencapsulated mutant was easily ingested by macrophages. On the other hand, the well encapsulated GBS strain and its unencapsulated mutant were both phagocytosed in large numbers. Even if S. suis unencapsulated mutant showed a higher uptake rate than the parental strain, this value was always markedly lower than the numbers of ingested GBS strains. In addition, the intracellular survival of encapsulated and unencapsulated GBS strains was significantly higher than that of S. suis strains. These results suggest that interactions between GBS type III and S. suis type 2 with murine macrophages as well as the role of the capsule as an antiphagocytic factor are different for the two bacterial pathogens.

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“…Complement-dependent phagocytosis is mediated by the CR3 (CD11b/CD18, ␣ M ␤ 2 ), which belongs to the ␤ 2 -integrin family, and it was shown that CD11b is critical for the recognition of C3bi [38], the activation product of C3. Additionally, CR3 can recognize microbes, e.g., type B streptococci, by interacting directly with molecules on their surface [39]. As SFKs are downstream of the CR3 pathway [40], we investigated the effect of CR3 (CD11b Ϫ/Ϫ ) deficiency in pneumoccocal meningitis to explore the functional differences between the two strains.…”

Section: Discussionmentioning

confidence: 99%

Myeloid Src kinases regulate phagocytosis and oxidative burst in pneumococcal meningitis by activating NADPH oxidase

Paul

Obermaier

Ziffle

et al. 2008

Journal of Leukocyte Biology

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Myeloid cells, including neutrophils and macrophages, play important roles in innate immune defense against acute bacterial infections. Myeloid Src family kinases (SFKs) p59/61(hck) (Hck), p58(c-fgr) (Fgr), and p53/56(lyn) (Lyn) are known to control integrin beta(2) signal transduction and FcgammaR-mediated phagocytosis in leukocytes. In this study, we show that leukocyte recruitment into the cerebrospinal fluid space and bacterial clearance is hampered in mice deficient in all three myeloid SFKs (hck(-/-)fgr(-/-)lyn(-/-)) during pneumococcal meningitis. As a result, the hck(-/-)fgr(-/-)lyn(-/-) mice developed increased intracranial pressure and a worse clinical outcome (increased neurologic deficits and mortality) compared with wild-type mice. Impaired bacterial killing was associated with a lack of phagocytosis and superoxide production in triple knockout neutrophils. Moreover, in hck(-/-)fgr(-/-)lyn(-/-) neutrophils, phosphorylation of p40(phox) was absent in response to pneumococcal stimulation, indicating a defect in NAPDH oxidase activation. Mice lacking the complement receptor 3 (CR3; CD11b/CD18), which belongs to the beta(2)-integrin family, also displayed impaired host defense against pneumococci, along with defective neutrophil superoxide production, but cerebrospinal fluid pleocytosis was normal. Cerebral expression of cytokines and chemokines was not decreased in both mouse strains, indicating that CR3 and myeloid SFKs are dispensable for the production of inflammatory mediators. Thus, our study demonstrates the pivotal role of myeloid SFKs and CR3 in mounting an effective defense against CNS infection with Streptococcus pneumonia by regulating phagocytosis and NADPH oxidase-dependent superoxide production. These data support the role of SFKs as critical mediators of CR3 signal transduction in host defense.

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Opsonin-independent phagocytosis of group B streptococci: role of complement receptor type three

Cited by 39 publications

References 43 publications

Nonopsonic binding of Mycobacterium tuberculosis to human complement receptor type 3 expressed in Chinese hamster ovary cells

Nonopsonic binding of Mycobacterium tuberculosis to human complement receptor type 3 expressed in Chinese hamster ovary cells

Streptococcus suis and group B Streptococcus differ in their interactions with murine macrophages

Myeloid Src kinases regulate phagocytosis and oxidative burst in pneumococcal meningitis by activating NADPH oxidase

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