AI Article Synopsis
- Macrophage-derived inflammatory cytokines play a crucial role in fighting T. marneffei infections in HIV/AIDS patients, but too many cytokines can lead to worse outcomes for the disease.
- The study found that T. marneffei triggers pyroptosis in macrophages via the NLRP3/caspase-1 pathway, and that the drug thalidomide enhances this process in infected macrophages.
- While thalidomide helped reduce inflammation in T. marneffei-infected mice, combining it with amphotericin B did not improve overall survival compared to using amphotericin B alone.
Article Abstract
Macrophage-derived inflammatory cytokines are critical for host defense against Talaromyces marneffei (T. marneffei) infection among HIV/AIDS patients, and excessive inflammatory cytokines are associated with poor outcomes of AIDS-associated talaromycosis. However, the underlying mechanisms of macrophage-caused pyroptosis and cytokine storm are poorly understood. Here, in the T. marneffei-infected mice and macrophages, we show that T. marneffei induced pyroptosis in macrophages through the NLRP3/caspase-1 pathway. The immunomodulatory drug thalidomide could promote the pyroptosis of macrophages infected T. marneffei. In T. marneffei-infected mice, the splenic macrophages underwent increasing pyroptosis as talaromycosis deteriorated. Thalidomide ameliorated inflammation of mice, while amphotericin B (AmB) in combination with thalidomide did not improve overall survival compared with AmB alone. Taken together, our findings suggest that thalidomide promotes NLRP3/caspase-1-mediated pyroptosis of macrophages in T. marneffei infection.
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| http://dx.doi.org/10.1016/j.micpath.2023.106168 | DOI Listing |
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