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Infection and Immunity, November 2001, p. 6796-6803, Vol. 69, No. 11
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.11.6796-6803.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Capsule Production and Growth Phase Influence Binding of Complement to Staphylococcus aureus

K. M. Cunnion,1,* J. C. Lee,2 and M. M. Frank1

Department of Pediatrics, Duke University Medical Center, Durham, North Carolina 27710,1 and Channing Laboratory, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115-58042

Received 7 March 2001/Returned for modification 10 May 2001/Accepted 24 July 2001

Complement-mediated opsonization of bacteria by C3 binding is an important component of the host innate immune system. Little information is available concerning the interaction between complement proteins and capsule type 5 and 8 Staphylococcus aureus strains, even though these isolates are responsible for ~70% of human staphylococcal infections. To investigate the importance of an intact complement pathway in an experimental staphylococcal infection, control and C3-depleted mice were challenged intravenously with 107 CFU of a serotype 5 S. aureus isolate. Whereas only 8% of the control mice succumbed to the infection, 64% of the complemented-depleted animals died. In vitro parameters of C3 binding to two heavily encapsulated (CP++) strains, three encapsulated (CP+) strains, and an isogenic capsule-negative (CP-) mutant were examined. The alternative pathway contributed 90% of C3 binding in 20% serum at 30 min, whereas it accounted for only 13% of C3 binding in 2% serum. Stationary-phase organisms bound only 10% as much C3 as mid-log-phase organisms; this was only in part due to capsule. When the S. aureus strains were cultivated on solid medium, the CP++ isolates bound 50% less C3 than CP+ strains; a CP+ strain bound 42% less C3 than the CP- mutant. Both C3b and iC3b fragments of C3 bound to S. aureus cells, and about one-third of the bound C3 was shed from the staphylococcal surface as iC3b, regardless of the CP phenotype of the strain. Thus, the phase of growth and presence of capsule are critical to opsonization.

* Corresponding author. Mailing address: Department of Pediatrics, Duke University Medical Center, Box 3499, 137 Medical Science Research Building, Durham, NC 27710. Phone: (919) 681-8904. Fax: (919) 681-8514. E-mail: Cunni003{at}mc.duke.edu.

Infection and Immunity, November 2001, p. 6796-6803, Vol. 69, No. 11
0019-9567/01/$04.00+0   DOI: 10.1128/IAI.69.11.6796-6803.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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