期刊
JOURNAL OF IMMUNOLOGY
卷 204, 期 12, 页码 3329-3338出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.2000159
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资金
- National Institutes of Health (NIH) [K22 AI116727]
- NIH [2T32AI007496-21]
Toxoplasma gondii is an obligate intracellular parasite that establishes life-long infection in a wide range of hosts, including humans and rodents. To establish a chronic infection, pathogens often exploit the trade-off between resistance mechanisms, which promote inflammation and kill microbes, and tolerance mechanisms, which mitigate inflammatory stress. Signaling through the type I IL-1R has recently been shown to control disease tolerance pathways in endotoxemia and Salmonella infection. However, the role of the IL-1 axis in T. gondii infection is unclear. In this study we show that IL-1R(-/-) mice can control T. gondii burden throughout infection. Compared with wild-type mice, IL-1R(-/-) mice have more severe liver and adipose tissue pathology during acute infection, consistent with a role in acute disease tolerance. Surprisingly,IL-1R(-/-) mice had better long-term survival than wild-type mice during chronic infection. This was due to the ability of IL-1R(-/-) mice to recover from cachexia, an immune-metabolic disease of muscle wasting that impairs fitness of wild-type mice. Together, our data indicate a role for IL-1R as a regulator of host homeostasis and point to cachexia as a cost of long-term reliance on IL-1-mediated tolerance mechanisms.
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