A fibrinogen-binding lipoprotein contributes to the virulence of Haemophilus ducreyi in humans

Margaret E. Bauer; Carisa A. Townsend; Ryan S. Doster; Kate R. Fortney; Beth W. Zwickl; Barry P. Katz; Stanley M. Spinola; Diane M. Janowicz

doi:10.1086/596656

A fibrinogen-binding lipoprotein contributes to the virulence of Haemophilus ducreyi in humans

Margaret E. Bauer, Carisa A. Townsend, Ryan S. Doster, Kate R. Fortney, Beth W. Zwickl, Barry P. Katz, Stanley M. Spinola, Diane M. Janowicz

Research output: Contribution to journal › Article › peer-review

23 Scopus citations

Abstract

A gene expression study of Haemophilus ducreyi identified the hypothetical lipoprotein HD0192, renamed here "fibrinogen binder A" (FgbA), as being preferentially expressed in vivo. To test the role played by fgbA in virulence, an isogenic fgbA mutant (35000HPfgbA) was constructed using H. ducreyi 35000HP, and 6 volunteers were experimentally infected with 35000HP or 35000HPfgbA. The overall pustule-formation rate was 61.1% at parent sites and 22.2% at mutant sites (P = .019). Papules were significantly smaller at mutant sites than at parent sites (13.3 vs. 37.9 mm²; P = .002) 24 h after inoculation. Thus, fgbA contributed significantly to the virulence of H. ducreyi in humans. In vitro experiments demonstrated that fgbA encodes a fibrinogen-binding protein; no other fibrinogen-binding proteins were identified in 35000HP. fgbA was conserved among clinical isolates of both class I and II H. ducreyi strains, supporting the finding that fgbA is important for H. ducreyi infection.

Original language	English (US)
Pages (from-to)	684-692
Number of pages	9
Journal	Journal of Infectious Diseases
Volume	199
Issue number	5
DOIs	https://doi.org/10.1086/596656
State	Published - Mar 1 2009

ASJC Scopus subject areas

Immunology and Allergy
Infectious Diseases

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10.1086/596656

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A fibrinogen-binding lipoprotein contributes to the virulence of Haemophilus ducreyi in humans. / Bauer, Margaret E.; Townsend, Carisa A.; Doster, Ryan S.; Fortney, Kate R.; Zwickl, Beth W.; Katz, Barry P.; Spinola, Stanley M.; Janowicz, Diane M.

In: Journal of Infectious Diseases, Vol. 199, No. 5, 01.03.2009, p. 684-692.

Research output: Contribution to journal › Article › peer-review

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title = "A fibrinogen-binding lipoprotein contributes to the virulence of Haemophilus ducreyi in humans",

abstract = "A gene expression study of Haemophilus ducreyi identified the hypothetical lipoprotein HD0192, renamed here {"}fibrinogen binder A{"} (FgbA), as being preferentially expressed in vivo. To test the role played by fgbA in virulence, an isogenic fgbA mutant (35000HPfgbA) was constructed using H. ducreyi 35000HP, and 6 volunteers were experimentally infected with 35000HP or 35000HPfgbA. The overall pustule-formation rate was 61.1% at parent sites and 22.2% at mutant sites (P = .019). Papules were significantly smaller at mutant sites than at parent sites (13.3 vs. 37.9 mm2; P = .002) 24 h after inoculation. Thus, fgbA contributed significantly to the virulence of H. ducreyi in humans. In vitro experiments demonstrated that fgbA encodes a fibrinogen-binding protein; no other fibrinogen-binding proteins were identified in 35000HP. fgbA was conserved among clinical isolates of both class I and II H. ducreyi strains, supporting the finding that fgbA is important for H. ducreyi infection.",

author = "Bauer, {Margaret E.} and Townsend, {Carisa A.} and Doster, {Ryan S.} and Fortney, {Kate R.} and Zwickl, {Beth W.} and Katz, {Barry P.} and Spinola, {Stanley M.} and Janowicz, {Diane M.}",

note = "Funding Information: Financial support: National Institute of Allergy and Infectious Disease (Public Health Service grants R01 AI27863 [to S.M.S.], U19 AI31494 [to S.M.S.], K08 AI74657 [to D.M.J.], and T32 AI07637 [to D.M.J.]), National Institutes of Health (grant M01 RR00750 to the General Clinic Research Center at Indiana University); Indiana University–Purdue University at Indianapolis (Research Support Funds grant [to M.E.B.] and Biomedical Research grant [to M.E.B.]); Indiana Genomics Initiative of Indiana University (to M.E.B.), which is supported in part by Lilly Endowment, Inc.",

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AU - Bauer, Margaret E.

AU - Townsend, Carisa A.

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AU - Katz, Barry P.

AU - Spinola, Stanley M.

AU - Janowicz, Diane M.

N1 - Funding Information: Financial support: National Institute of Allergy and Infectious Disease (Public Health Service grants R01 AI27863 [to S.M.S.], U19 AI31494 [to S.M.S.], K08 AI74657 [to D.M.J.], and T32 AI07637 [to D.M.J.]), National Institutes of Health (grant M01 RR00750 to the General Clinic Research Center at Indiana University); Indiana University–Purdue University at Indianapolis (Research Support Funds grant [to M.E.B.] and Biomedical Research grant [to M.E.B.]); Indiana Genomics Initiative of Indiana University (to M.E.B.), which is supported in part by Lilly Endowment, Inc.

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N2 - A gene expression study of Haemophilus ducreyi identified the hypothetical lipoprotein HD0192, renamed here "fibrinogen binder A" (FgbA), as being preferentially expressed in vivo. To test the role played by fgbA in virulence, an isogenic fgbA mutant (35000HPfgbA) was constructed using H. ducreyi 35000HP, and 6 volunteers were experimentally infected with 35000HP or 35000HPfgbA. The overall pustule-formation rate was 61.1% at parent sites and 22.2% at mutant sites (P = .019). Papules were significantly smaller at mutant sites than at parent sites (13.3 vs. 37.9 mm2; P = .002) 24 h after inoculation. Thus, fgbA contributed significantly to the virulence of H. ducreyi in humans. In vitro experiments demonstrated that fgbA encodes a fibrinogen-binding protein; no other fibrinogen-binding proteins were identified in 35000HP. fgbA was conserved among clinical isolates of both class I and II H. ducreyi strains, supporting the finding that fgbA is important for H. ducreyi infection.

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