Amoebae skin nibblers causing disease by displaying host cell proteins

A parasitic amoeba causing severe intestinal disease in humans protects itself from attacks by biting host cell fragments and depositing their proteins at its own surface, according to a study by microbiologists at the University of California in Davis.

"We are very excited about the links between amoeba infection and the broader themes of cell biology," said Katherine Ralston, assistant professor in the Department of Microbiology and Molecular Genetics at the College of Biological Sciences. An article describing the work appears today (April 30) in the newspaper mbio.

Entamoeba histolytica causes severe diarrheal disease, mainly in tropical countries. He lives in the intestines, causing ulcers and bleeding. In severe cases, it can burst and invade other organs.

Ralston studied Entamoeba during postdoctoral work at the University of Virginia. Amoeba and many other cells, including some that protect us from the disease, are known to "eat" other cells by completely engulfing them, a process called phagocytosis.

Ralston discovered that Entamoeba could also pinch small pieces of human cells. She called this process trogocytosis or "cell nibbling".

"The amoeba literally removes bites from other cells," Ralston said. "This nibbling is the way it attacks individual cells, and we think it is so that it causes ulceration and damage to the human gut."

Cell nibbling has also been described in other parasitic amoebae, as well as in multicellular organisms. Cells of the immune system, for example, can exchange parts of their surface by biting them.

"We thought that if amoebae could extract proteins from host cells and put them on their surface, that would have a functional effect on their survival in the body," said graduate student Hannah Miller.

Complement camouflage

The body produces a set of proteins in the blood, called "complement", which can attack parasites and bacteria. Your own cells carry proteins that prevent them from being attacked by the complement.

Miller, Ralston and René Suleiman, another graduate student in the lab, discovered that when amoebae were in contact with human cells, they could take these protective proteins and coat them as a sort of "complement camouflage". The common Entamoebae were killed by human serum, but the amoebae that had camouflaged themselves survived.

This camouflage could protect them from the supplement as they migrate into the blood around the body, Miller said.

Miller and Ralston are now trying to understand what proteins are transferred, how they interact with the supplement and what happens to these proteins once they've been nibbled in another cell. Do they go directly into the amoeba membrane, or are they treated internally first?

They also want to know more about trogocytosis in general. Why are some cases mild, while others lead to cell death? The process can also be important for understanding how cancer cells behave and how they can be killed.

"We're really excited that this protein-based decoration can be applied to trogocytosis in general because we realize that it is important in many settings," Ralston said.