Data Sheet 1_Targeting the capsule of Klebsiella pneumoniae with a cationic CR3-binding protein enhances phagocytosis and promotes bacterial clearance and survival in a mouse sepsis model.pdf

It also increased phagocytosis of carbapenem-resistant K. pneumoniae. rPF4 did not directly kill bacteria but acted as an opsonin, binding to the negatively charged bacterial capsule and creating recognition sites for CR3 on leukocytes. In a mouse sepsis model, a single dose of rPF4 significantly enhanced bacterial clearance from the lungs, liver, and peritoneum and reduced bacteremia. Histological analyses showed that rPF4 provided substantial protection to lung and liver tissues against K. pneumoniae-induced damage.

Consistent with these findings, rPF4 treatment increased the survival rates of infected mice. These results show that rPF4 effectively targets the capsule, a key virulence factor of K. pneumoniae, thereby reducing the bacterium’s ability to evade the host immune response. Overall, the data suggest a common mechanism in which cationic rPF4, by binding to the negatively charged surfaces of both Gram-negative and Gram-positive bacteria, diminishes their antiphagocytic properties.</p>