Evaluation of an isogenic hemolysin-deficient mutant in the human model of Haemophilus ducreyi infection

K. L. Palmer; A. C. Thornton; K. R. Fortney; A. F. Hood; R. S. Munson; S. M. Spinola

doi:10.1086/515617

Evaluation of an isogenic hemolysin-deficient mutant in the human model of Haemophilus ducreyi infection

K. L. Palmer
, A. C. Thornton
, K. R. Fortney
, A. F. Hood
, R. S. Munson
, S. M. Spinola

Producción científica: Article › revisión exhaustiva

40 Citas (Scopus)

Resumen

Haemophilus ducreyi causes the genital ulcerative disease chancroid. One putative virulence factor of H. ducreyi is a pore-forming hemolysin that displays toxicity against human fibroblasts and keratinocytes. In order to test the role of the hemolysin in pathogenesis, an isogenic hemolysin- deficient mutant was constructed, designated 35000HP-RSM1. The lipooligosaccharide, outer membrane protein patterns, and growth attributes of 35000HP-RSM1 were identical to its parent, 35000HP. Human subjects were challenged on the upper arm with the isogenic isolates in a double-blinded, randomized, escalating dose-response study. Pustules developed at a similar rate at sites inoculated with the mutant or parent. The cellular infiltrate and bacterial load in lesions were also similar. These results indicate the hemolysin does not play a role in pustule formation. Due to the limitations of this model, the role of the hemolysin at later stages of infection could not be determined.

Idioma original	English
Páginas (desde-hasta)	191-199
Número de páginas	9
Publicación	Journal of Infectious Diseases
Volumen	178
N.º	1
DOI	https://doi.org/10.1086/515617
Estado	Published - 1998

Nota bibliográfica

Funding Information:
Received 22 September 1997; revised 11 February 1998. Presented in part: International Congress of Sexually Transmitted Diseases, Seville, Spain, October 1997. Informed consent was obtained from the subjects for participation and for HIV serology, in accordance with the human experimentation guidelines of the US Department of Health and Human Services and the Institutional Review Board of Indiana University-Purdue University at Indianapolis. Grant support: NIH (AI-34967, AI-27863, AI-30006, RR-00750, and T32DK-07532). Reprints or correspondence: Dr. Stanley M. Spinola, Indiana University School of Medicine, Dept. of Medicine, Emerson Hall, Room 435, 545 Barnhill Dr., Indianapolis, IN 46202 ([email protected]).

Financiación

Received 22 September 1997; revised 11 February 1998. Presented in part: International Congress of Sexually Transmitted Diseases, Seville, Spain, October 1997. Informed consent was obtained from the subjects for participation and for HIV serology, in accordance with the human experimentation guidelines of the US Department of Health and Human Services and the Institutional Review Board of Indiana University-Purdue University at Indianapolis. Grant support: NIH (AI-34967, AI-27863, AI-30006, RR-00750, and T32DK-07532). Reprints or correspondence: Dr. Stanley M. Spinola, Indiana University School of Medicine, Dept. of Medicine, Emerson Hall, Room 435, 545 Barnhill Dr., Indianapolis, IN 46202 ([email protected]).

Financiadores	Número del financiador
National Institutes of Health (NIH)	RR-00750, AI-30006, AI-27863, T32DK-07532
National Institute of Allergy and Infectious Diseases	R01AI034967

ODS de las Naciones Unidas

Este resultado contribuye a los siguientes Objetivos de Desarrollo Sostenible

Good health and well being

ASJC Scopus subject areas

Immunology and Allergy
Infectious Diseases

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10.1086/515617

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title = "Evaluation of an isogenic hemolysin-deficient mutant in the human model of Haemophilus ducreyi infection",

abstract = "Haemophilus ducreyi causes the genital ulcerative disease chancroid. One putative virulence factor of H. ducreyi is a pore-forming hemolysin that displays toxicity against human fibroblasts and keratinocytes. In order to test the role of the hemolysin in pathogenesis, an isogenic hemolysin- deficient mutant was constructed, designated 35000HP-RSM1. The lipooligosaccharide, outer membrane protein patterns, and growth attributes of 35000HP-RSM1 were identical to its parent, 35000HP. Human subjects were challenged on the upper arm with the isogenic isolates in a double-blinded, randomized, escalating dose-response study. Pustules developed at a similar rate at sites inoculated with the mutant or parent. The cellular infiltrate and bacterial load in lesions were also similar. These results indicate the hemolysin does not play a role in pustule formation. Due to the limitations of this model, the role of the hemolysin at later stages of infection could not be determined.",

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note = "Funding Information: Received 22 September 1997; revised 11 February 1998. Presented in part: International Congress of Sexually Transmitted Diseases, Seville, Spain, October 1997. Informed consent was obtained from the subjects for participation and for HIV serology, in accordance with the human experimentation guidelines of the US Department of Health and Human Services and the Institutional Review Board of Indiana University-Purdue University at Indianapolis. Grant support: NIH (AI-34967, AI-27863, AI-30006, RR-00750, and T32DK-07532). Reprints or correspondence: Dr. Stanley M. Spinola, Indiana University School of Medicine, Dept. of Medicine, Emerson Hall, Room 435, 545 Barnhill Dr., Indianapolis, IN 46202 ([email protected]).",

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AU - Hood, A. F.

AU - Munson, R. S.

AU - Spinola, S. M.

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N2 - Haemophilus ducreyi causes the genital ulcerative disease chancroid. One putative virulence factor of H. ducreyi is a pore-forming hemolysin that displays toxicity against human fibroblasts and keratinocytes. In order to test the role of the hemolysin in pathogenesis, an isogenic hemolysin- deficient mutant was constructed, designated 35000HP-RSM1. The lipooligosaccharide, outer membrane protein patterns, and growth attributes of 35000HP-RSM1 were identical to its parent, 35000HP. Human subjects were challenged on the upper arm with the isogenic isolates in a double-blinded, randomized, escalating dose-response study. Pustules developed at a similar rate at sites inoculated with the mutant or parent. The cellular infiltrate and bacterial load in lesions were also similar. These results indicate the hemolysin does not play a role in pustule formation. Due to the limitations of this model, the role of the hemolysin at later stages of infection could not be determined.

AB - Haemophilus ducreyi causes the genital ulcerative disease chancroid. One putative virulence factor of H. ducreyi is a pore-forming hemolysin that displays toxicity against human fibroblasts and keratinocytes. In order to test the role of the hemolysin in pathogenesis, an isogenic hemolysin- deficient mutant was constructed, designated 35000HP-RSM1. The lipooligosaccharide, outer membrane protein patterns, and growth attributes of 35000HP-RSM1 were identical to its parent, 35000HP. Human subjects were challenged on the upper arm with the isogenic isolates in a double-blinded, randomized, escalating dose-response study. Pustules developed at a similar rate at sites inoculated with the mutant or parent. The cellular infiltrate and bacterial load in lesions were also similar. These results indicate the hemolysin does not play a role in pustule formation. Due to the limitations of this model, the role of the hemolysin at later stages of infection could not be determined.

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Evaluation of an isogenic hemolysin-deficient mutant in the human model of Haemophilus ducreyi infection

Resumen

Nota bibliográfica

Financiación

ODS de las Naciones Unidas

ASJC Scopus subject areas

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