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Increased Amounts of the Aspergillus Metabolite D-Mannito! in Tissue and Serum of Rats with Experimental Aspergillosis

  • Brian Wong
  • , Karen L. Brauer
  • , Ring R. Tsai
  • , Koka Jayasimhulu

Research output: Contribution to journalArticlepeer-review

Abstract

Several Aspergillus species produce large amounts of the hexitol d-rnannitol in vitro, but it is not known whether these species also produce d-rnannitol in vivo. Serum samples and homogenized tissues were analyzed from rats pretreated with cortisone and cyclophosphamide and then given 2 × 106 preincubated conidia of Aspergillus jumigatus intravenously. The resulting infection was lethal by 48 h and was characterized by much more severe disease in the liver than in the kidneys, spleen, or lungs. A compound present in increased amounts in the livers and sera of the infected rats was shown to be d-mannitol by gas chromatography (GC) and GC/mass spectrometry and enzymatically. Quantitative analysis by GC showed that the infected rats had more d-mannitol in their livers (but not in their lungs or kidneys) after 12 h (P <.01 at 12, 24, and 36 h) and higher serum d-mannitol concentrations and serum d-mannitol/creatinine ratios after 36 h (P <.05) than did uninfected controls. These results indicate that A. jumigatus can produce and release sufficient d-mannitol in the tissues of infected animals to raise serum d-mannitol levels. Thus, d-mannitol is a potential diagnostic marker for aspergillosis.

Original languageEnglish (US)
Pages (from-to)95-103
Number of pages9
JournalJournal of Infectious Diseases
Volume160
Issue number1
DOIs
StatePublished - Jul 1989
Externally publishedYes

Funding

Receivedfor publication 26September 1988and in revisedform 15 February 1989. This work was presented in part at the 34th Annual Conference on Mass Spectrometry and Related Topics, held on 13June 1986in Cincinnati, Ohio, and at the 26th ICAAC, held from 28 October to I November 1986 in New Orleans, Louisiana. This work was supported by grant AI-23938 from the National Institute of Allergy and Infectious Diseases and by the University Research Council of the University of Cincinnati. The authors thank Sandra Beggs for technical assistance. Please address requests for reprints to Dr. Brian Wong, Department of Internal Medicine, University of Cincinnati College of Medicine, 231 Bethesda Ave., Cincinnati, OH 45267-0560.

FundersFunder number
University Research Council of the University of Cincinnati
National Institute of Allergy and Infectious DiseasesR01AI023938

    ASJC Scopus subject areas

    • Immunology and Allergy
    • Infectious Diseases

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