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Infection and Immunity, November 1998, p. 5215-5223, Vol. 66, No. 11
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Neisseria gonorrhoeae Heme Biosynthetic Mutants Utilize Heme and Hemoglobin as a Heme Source but Fail To Grow within Epithelial Cells

Paul C. Turner,1,* Christopher E. Thomas,1 Christopher Elkins,1,2 Susan Clary,3 and P. F. Sparling1,2

Department of Medicine, School of Medicine,1 and Department of Microbiology and Immunology,2 University of North Carolina, Chapel Hill, North Carolina 27599, and Department of Molecular Microbiology and Immunology, Oregon Health Sciences University, Portland, Oregon 972013

Received 29 April 1998/Returned for modification 12 June 1998/Accepted 29 July 1998

Many bacterial pathogens, including pathogenic neisseriae, can use heme as an iron source for growth. To study heme utilization by Neisseria gonorrhoeae, two heme biosynthetic mutants were constructed, one with a mutation in hemH (the gene encoding ferrochelatase) and one with a mutation in hemA (the gene encoding gamma -glutamyl tRNA reductase). The hemH mutant failed to grow without an exogenous supply of heme or hemoglobin, whereas the hemA mutant failed to grow unless heme, hemoglobin, or heme precursors were present. Growth of the mutants with hemoglobin required expression of the hemoglobin receptor (HpuAB) and was TonB dependent. However, growth with heme required neither HpuAB nor TonB. An fbpA mutant grew normally when either heme or hemoglobin was present in the medium. The heme biosynthetic mutants showed reduced intracellular survival, compared to the parent strain, within A-431 endocervical epithelial cell cultures. These studies demonstrate that in addition to synthesizing their own heme, N. gonorrhoeae strains are able to internalize and utilize exogenous heme independently of FbpA but appear unable to obtain heme from within epithelial cells for growth.

* Corresponding author. Mailing address: Department of Medicine, Division of Infectious Diseases, University of North Carolina at Chapel Hill, 521 Burnett-Womack Bldg., CB 7030, Chapel Hill, NC 27599. Phone: (919) 966-3661. Fax: (919) 966-6714. E-mail: pturner{at}med.unc.edu.

Infection and Immunity, November 1998, p. 5215-5223, Vol. 66, No. 11
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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