Significance The work summarized in this paper is based on the simple but unexpected observation that addition of lipopolysaccharide (LPS) or bacteria to human wound fluids leads to precipitation of protein aggregates, a phenomenon not observed in plasma. Using a broad mix of technologies ranging from biophysical, biochemical, and microbiological methods to fluorescence and electron microscopy, and from in silico modeling to studies on wound materials, we demonstrate here a previously undisclosed role of C-terminal thrombin fragments of about 11 kDa, involving LPS- and bacteria-induced aggregation and scavenging, facilitating clearance and microbial killing. Our findings provide a link between the major coagulation factor thrombin, innate immunity, and amyloid formation.