AFAP-1L1-mediated actin filaments crosslinks hinder Trypanosoma cruzi cell invasion and intracellular multiplication

Knocking-down AFAP-1L1 increased Trypanosoma cruzi cell invasion and intracellular multiplication. Thus, we have shown that the integrity of the machinery formed by AFAP-1L1 in actin cytoskeleton polymerization is important to hinder parasite infection. [Display omitted] •AFAP-1L1 forms a physical barrier to Trypanosoma cruzi cell invasion and intracellular multiplication.•Knocking-down AFAP-1L1 induces softening of actin filaments.•Knocking-down AFAP-1L1 facilitates T. cruzi cell invasion and intracellular multiplication. Host actin cytoskeleton polymerization has been shown to play an important role during Trypanosoma cruzi internalization into mammalian cell. The structure and dynamics of the actin cytoskeleton in cells are regulated by a vast number of actin-binding proteins. Here we aimed to verify the impact of AFAP-1L1, during invasion and multiplication of T. cruzi. Knocking-down AFAP-1L1 increased parasite cell invasion and intracellular multiplication. Thus, we have shown that the integrity of the machinery formed by AFAP-1L1 in actin cytoskeleton polymerization is important to hinder parasite infection.