



Researchers studying lupus in mice found that chronic inflammation redirects neutrophils, the immune cells that normally respond first to bacterial infection, toward a faster but less effective defensive response. Inflammatory signals reduced the cells' ability to sense a bacterial chemical marker that normally triggers a more potent antibacterial trap, pushing them instead toward a quicker version that spares the cell but kills fewer bacteria.
The team found standard lupus treatments could correct some of these cellular defects and reduce bacteria in several organs, though this did not significantly improve survival in lupus-prone mice compared with untreated animals. The findings help explain why serious infection remains a persistent risk for lupus patients even though their immune systems are, by most measures, overactive.
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