IL-12 protects mice against pulmonary and disseminated infection caused by Cryptococcus neoformans

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Abstract
We examined the role of IL‐12 in host resistance to Cryptococcus neoformans using a murine model of pulmonary and disseminated infection. In this model, mice were infected intratracheally with viable yeast cells. Mice untreated with IL‐12 allowed an uncontrolled multiplication of yeast cells in the lung with infiltrations of few inflammatory cells, and a cryptococcal dissemination to the brain and meningitis by 3 weeks, resulting in death of all animals within 4–6 weeks. IL‐12, when administered from the day of tracheal infection for 7 days, induced a marked infiltration of inflammatory cells, consisting mostly of mononuclear cells, and significantly reduced the number of viable yeast cells in the lung. The treatment suppressed brain dissemination, as shown by a marked reduction of yeast cells in the brain and prevention of meningitis. These effects resulted in a significant increase in the survival rate of infected mice. In contrast, late administration of IL‐12 commencing on day 7 after instillation of yeast cells failed to protect the mice against infection with C. neoformans. In further experiments, early administration of IL‐12 markedly induced interferon‐gamma (IFN‐γ) mRNA in the lungs of infected mice, while no IFN‐γ mRNA was detected without this treatment. Our results indicate that IL‐12 is effective when administered in the early period of pulmonary cryptococcal infection.

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