Research Article

Effect of glucan on Leishmania major infection in BALB/c mice

Journal of Medical Microbiology 1987; 23(4):363

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Summary auto-generated

This study examined whether glucan, a β-1,3 polysaccharide immunomodulator derived from yeast cell walls, could reduce Leishmania major infection in highly susceptible BALB/c mice. Researchers administered glucan (0.45 mg) or control dextrose intraperitoneally four times before subcutaneous infection with L. major promastigotes. Parasite burden was assessed in liver and spleen at 3, 5, 6, 8, and 10 weeks post-infection by counting amastigotes in tissue sections. Glucan pretreatment significantly reduced parasite proliferation in both organs at weeks 4, 6, and 8 compared to controls (p < 0.01), with amastigotes appearing later in glucan-treated spleens. However, this protective effect disappeared by week 10, likely due to loss of glucan potency over time. The authors suggest glucan-activated macrophages suppress parasite multiplication through non-specific immune mechanisms, possibly involving increased lysozyme release. The findings support glucan's immunostimulatory potential against visceral leishmaniasis caused by L. major, though the temporary nature of protection limits clinical application.

Key findings

  • Glucan pretreatment significantly reduced L. major amastigote proliferation in liver and spleen at 4, 6, and 8 weeks post-infection (p < 0.01)
  • Parasite burden in glucan-treated mice peaked later than controls and remained lower through week 8, but protection was lost by week 10
  • Non-specific activation of macrophages by glucan appears to enhance parasite killing, possibly through increased lysozyme production within phagosomes
  • The temporary protective effect suggests glucan potency diminishes over the infection course, limiting its sustained therapeutic value

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Abstract

The effect of glucan on Leishmania major infection was studied in BALB/c mice, which are highly susceptible to leishmania infection. Glucan (0.45 mg), or isovolumetric dextrose, was administered intraperitoneally 7, 5, 3 and 1 day before infection with L. major promastigotes. At 3, 5, 6, 8 and 10 weeks after infection, animals were killed; the liver and spleen of each animal were weighed and the parasite burden was calculated. A significant (p less than 0.01) reduction in amastigote proliferation in liver and spleen of animals pretreated with glucan was demonstrated 4, 6 and 8 weeks after infection.