Using GIS to Prioritize Green Infrastructure Installation Strategies in an Urbanized Watershed

2014 S.C. Water Resources Conference - Informing Strategic Water Planning to Address Natural Resource, Community and Economic Challenge

Watershed Plan Implementation Challenges for SMS4S in Murrells Inlet

2014 S.C. Water Resources Conference - Informing Strategic Water Planning to Address Natural Resource, Community and Economic Challenge

Evaluating the Role of Evapotranspirative Processes for Stormwater Management in Coastal South Carolina Watersheds with Shallow Groundwater

2014 S.C. Water Resources Conference - Informing Strategic Water Planning to Address Natural Resource, Community and Economic Challenge

Green Infrastructure in Coastal Landscapes: Ecological Design, Hydrological Function, and Sustainable Land Use Goals

2012 S.C. Water Resources Conference - Exploring Opportunities for Collaborative Water Research, Policy and Managemen

It\u27s a Small World: Enhancing Human Cognition through Virtual Dioramas

2008 S.C. Water Resources Conference - Addressing Water Challenges Facing the State and Regio

Determining Environmental Flow Regime in the Pee Dee Watershed, SC

2010 South Carolina Water Resource Conference. Informing strategic water planning to address natural resource, community and economic challenges

Inflammation drives thrombosis after Salmonella infection via CLEC-2 on platelets

Thrombosis is a common, life-threatening consequence of systemic infection; however, the underlying mechanisms that drive the formation of infection-associated thrombi are poorly understood. Here, using a mouse model of systemic Salmonella Typhimurium infection, we determined that inflammation in tissues triggers thrombosis within vessels via ligation of C-type lectin-like receptor-2 (CLEC-2) on platelets by podoplanin exposed to the vasculature following breaching of the vessel wall. During infection, mice developed thrombi that persisted for weeks within the liver. Bacteria triggered but did not maintain this process, as thrombosis peaked at times when bacteremia was absent and bacteria in tissues were reduced by more than 90% from their peak levels. Thrombus development was triggered by an innate, TLR4-dependent inflammatory cascade that was independent of classical glycoprotein VI-mediated (GPVI-mediated) platelet activation. After infection, IFN-ã release enhanced the number of podoplanin-expressing monocytes and Kupffer cells in the hepatic parenchyma and perivascular sites and absence of TLR4, IFN-ã, or depletion of monocytic-lineage cells or CLEC-2 on platelets markedly inhibited the process. Together, our data indicate that infection-driven thrombosis follows local inflammation and upregulation of podoplanin and platelet activation. The identification of this pathway offers potential therapeutic opportunities to control the devastating consequences of infection-driven thrombosis without increasing the risk of bleeding