Role of polymorphonuclear leukocytes in the resistance of tumor-bearing mice against Candida albicans infection

Yoshio Okawa, Makiko Kobayashi, Kazuhiko Sakai, Masuko Suzuki

Research output: Contribution to journalArticle

3 Scopus citations


Tumor-bearing mice showed a significant resistance against Candida albicans intravenous infection. Longer survival was observed in groups of mice inoculated with fungal cells 2-3 weeks after tumor transplantation with allogeneic sarcoma 180, syngeneic methylcholanthrene-induced Meth A fibrosarcoma, and MM 46 mammary carcinoma than in non-tumor-bearing mice inoculated only with fungal cells. This effect was not observed when the mice were infected only 1 week after tumor transplantation. A significant decrease in the number of C. albicans cells in the kidneys was observed in mice inoculated with fungal cells 2-3 weeks after tumor transplantation. In the tumor-bearing mice treated with cyclophosphamide (CY), a remarkable decrease in both the number of peripheral blood polymorphonuclear leukocytes (PMNs) and the defense against challenge with C. albicans cells was observed, as compared with the CY-untreated groups (normal and tumor-bearing mice). A marked increase in the calcium concentration in serum and number, candidacidal activity, active oxygen level, and myeloperoxidase activity of PMNs was observed in the 2-3-week tumor-bearing mice. From these results, it is suggested that PMNs, which accumulated in the 2-3-week tumor-bearing mice, play an important role in the protection from C. albicans infection by increasing the number and the types of killing factors.

Original languageEnglish (US)
Pages (from-to)674-678
Number of pages5
JournalBiological and Pharmaceutical Bulletin
Issue number5
StatePublished - May 2004
Externally publishedYes



  • Candida albicans
  • Killing factor
  • Polymorphonuclear leukocyte
  • Protection against infection
  • Tumor-bearing mouse

ASJC Scopus subject areas

  • Molecular Medicine
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this