According to the World Health Organization, the number ofSalmonella infections is continuously rising, and the severity of infections is increasing. One of the reasons for this may be the sophisticated infection strategies the bacteria have evolved. The striking diversity of invasion strategies may allowSalmonella to infect multiple cell types and different hosts. Salmonella do not infect their hosts according to textbook model. Only a single infection mechanism has seriously been discussed in the field up till now -without understanding all the details.
Extensions of the cell membrane are filled with actin filaments. In the commonly accepted infection mechanism, Salmonellaabuses the Arp2/3 complex to enter the host cell: the bacteria activate the complex and thus initiate the formation actin filaments and development of prominent membrane extensions, so-called ruffles. These ruffles surround and enclose the bacteria so that they end up in the cell interior. Last year, the research groups headed by Theresia Stradal and Klemens Rottner discovered that Salmonella can also reach the cell interior without initiating membrane ruffles. With this, the researchers disproved a long-standing dogma.
All entry mechanisms employed by Salmonella target the so-called actin cytoskeleton of the host cell. Actin can polymerise into fine and dynamic fibrils, also called filaments, which associate into networks or fibres. These structures stabilise the cell and enable it to move, as they are constantly built up and taken down. One of the most important core elements is the Arp2/3 complex that nucleates the assembly of actin monomers into filaments.
In epithelial cells, the contractile structures are less organised but work similarly. Here, actin and myosin II form so-called stress fibres that tightly connect to the membrane. During an infection, stress fibres at the entry site can contract and pull the bacteria into the cell.
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