Evidence against a Role for Interleukin-10 in the Regulation of Growth of Mycobacterium avium in Human Monocytes

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Abstract
Interleukin-1O (IL-10) inhibits intracellular Mycobacterium avium killing by cytokine-activated murine macrophages and may have a role in pathogenesis. Cytokine activities in supernatants of M. avium-infected human monocytes were maximal at 6–24 h for tumor necrosis factor (TNF)-α and 24–48 h for IL-1O. TNF-α and IL-10 production increased with increasing M. avium-to-monocyte infection ratios (20:1 to 200:1). TNF-α production by monocytes infected with smooth, domed, and opaque organisms at 200:1 exceeded that of monocytes infected with smooth, flat, and transparent M. avium (P < .01). IL-10 induction demonstrated considerable strain-to-strain variability and did not correlate with intracellular M. avium growth. IL-10 significantly inhibited TNF-α, IL-1β, and IL-6 production by M. avium-infected monocytes. Coculturing monocytes with IL-10 after M. avium infection did not affect intracellular M. avium growth. Differential induction of TNF-α may be a factor in the intracellular growth of M. avium in human monocytes. IL-10, however, played no apparent role in pathogenicity in this model.

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