Scientists Find Potential Mechanism for Deadly, Sepsis-Induced Secondary Infection (IMAGE)
Caption
Skin TRM (seen in red) 'sense' infections and 'alarm' host tissue to recruit effector cells (green) to the skin where they contribute to viral clearance. Despite maintenance of skin TRM in septic hosts (CLP), tissue-wide recruitment of effector cells was greatly diminished resulting in enhanced susceptibility to secondary skin infections. Site-specific administration of chemokines (CXCL9-10) restored homing signals that were diminished in septic hosts to permit recruitment of effector cells to the skin. Thus, this approach could prove useful to enhance the septic patient's T-cell-mediated immunity during the period of immunosuppression.
Credit
Scott Anthony & Isaac Jensen at University of Iowa
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