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Infection and Immunity, April 1999, p. 1866-1870, Vol. 67, No. 4
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Capsular Sialic Acid Limits C5a Production on Type III Group B Streptococci

Shinji Takahashi,1 Youko Aoyagi,1 Elisabeth E. Adderson,2 Yoshiyuki Okuwaki,1 and John F. Bohnsack2,*

Department of Microbiology, Joshi-Eiyoh University, Sakado, Saitama, 350-0088, Japan,1 and Department of Pediatrics, University of Utah Health Sciences Center, Salt Lake City, Utah 841322

Received 15 September 1998/Returned for modification 17 November 1998/Accepted 19 January 1999

The majority of type III group B streptococcus (GBS) human neonatal infections are caused by a genetically related subgroup called III-3. We have proposed that a bacterial enzyme, C5a-ase, contributes to the pathogenesis of neonatal infections with GBS by rapidly inactivating C5a, a potent pro-inflammatory molecule, but many III-3 strains do not express C5a-ase. The amount of C5a produced in serum following incubation with representative type III strains was quantitated in order to better understand the relationship between C5a production and C5a-ase expression. C5a production following incubation of bacteria with serum depleted of antibody to the bacterial surface was inversely proportional to the sialic acid content of the bacterial capsule, with the more heavily sialylated III-3 strains generating less C5a than the less-virulent, less-sialylated III-2 strains. The amount of C5a produced correlated significantly with C3 deposition on each bacterial strain. Repletion with type-specific antibody caused increased C3b deposition and C5a production through alternative pathway activation, but C5a was functionally inactivated by strains that expressed C5a-ase. The increased virulence of III-3 strains compared to that of III-2 strains results at least partially from the higher sialic acid content of III-3 strains, which inhibits both opsonophagocytic killing and C5a production in the absence of type-specific antibody. We propose that C5a-ase is not necessary for III-3 strains to cause invasive disease because the high sialic acid content of III-3 strains inhibits C5a production.

* Corresponding author. Mailing address: Department of Pediatrics, Rm. 2A152, University of Utah Health Sciences Center, 50 North Medical Dr., Salt Lake City, UT 84132. Phone: (801) 581-5319. Fax: (801) 585-9314. E-mail: john.bohnsack{at}hsc.med.utah.edu.

Infection and Immunity, April 1999, p. 1866-1870, Vol. 67, No. 4
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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