The Actin Cytoskeleton and Bacterial Infection

Xenia Naj, Stefan Linder

The spirochete Borrelia burgdorferi is the causative agent of Lyme disease, a multisystemic disorder affecting primarily skin, nervous system, and joints. If an infection with Borrelia proceeds unchecked, the disease can also enter a chronic stage, leading to the development of neuroborreliosis or cardiac arrhythmia. Successful elimination of B. burgdorferi by the host immune system is thus decisive for the positive outcome of a respective infection. Accordingly, host immune cells such as macrophages and dendritic cells have to be able to efficiently internalize and degrade infecting spirochetes. These processes are based on closely controlled rearrangements of the actin cytoskeleton, which enables the spatiotemporally fine-tuned formation of cellular protrusions and compartments that assist in the capturing, immobilization, and uptake of borreliae, as well as their further intracellular processing. Here, we discuss actin-based structures, in particular filopodia and coiling pseudopods that are involved in phagocytosis of B. burgdorferi by macrophages, their regulation by actin-associated proteins such as formins and Arp2/3 complex, as well as the subsequent intracellular processing of borreliae.