Sanofi-Pasteur, the world’s biggest vaccine company, has signed a contract with the University of California, San Diego, to develop “an immunological approach to acne prevention and treatment”.
Acne is no joke. More than 85 per cent of teenagers and over 40 million people in the United States alone are suffering this disease” and many adults have it too, says Chun-Ming Huang, head of the lab at the centre of the deal.
Yet there is little effective treatment, says Huang. “This collaboration will make our dreams of acne vaccines for the public come true earlier.”
Benign bug turns nasty
Pimples develop when oil-producing sebaceous glands in the skin become clogged. As the oxygen level within the pore falls, some of its otherwise benign bacterial inhabitants turn nasty and start killing skin cells to break into the blood. In response the immune system unleashes local inflammation, bringing in white blood cells and germ-killing chemicals to battle the bacteria – creating a pimple.
The chief culprit is the main bacterium in sebaceous glands, Propionibacterium acnes. Current acne treatments, such as benzoyl peroxide and antibiotics, aim to kill the bacterium. But acne can be chronic, and long-term use of antibiotics can lead to drug resistance in P. acnes, while other antibacterials damage the skin – partly by killing off its normal bacteria.
A major obstacle in acne research has been the lack of test animals – mice and guinea pigs don’t get spots. Huang’s lab got round that by injecting P. acnes into the skin of a mouse’s ear, causing inflammation. In 2008 they reported that mice given simple nasal-spray vaccines containing whole, dead P. acnes, or a protein from its surface, showed reduced ear inflammation compared to unvaccinated mice when they were then given a live bacterial injection.
This showed that antibodies to P. acnes might reduce pimples. However, a stable community of normal skin bacteria is known to protects the skin from colonisation by nastier germs. A vaccine that encourages the body to indiscriminately attack P. acnes could cause worse trouble than acne.
So the team tried a different approach: targeting a protein called CAMP, which is used by various bacteria to kill host cells. The team found a CAMP gene in the DNA sequence of P. acnes, which coded for a protein that killed cells in sebaceous glands and triggered inflammation.
The team put the gene into young daikon radish plants, which duly made the protein. They then sprayed tiny amounts of the ground-up leaves into the noses of mice, which caused the mice to make antibodies to CAMP.
The team harvested the antibodies and added them to a colony of P. acnes in a dish, where the antibodies bound to the CAMP made by the bacteria and prevented its effects. When these bacteria were put in the skin of a mouse’s ear, they elicited much less inflammation than ordinary P. acnes.
Targeting the protein that the bacteria use to cause trouble, rather than killing the bacteria, is unlikely to encourage the selection of resistant bacteria, as all the P. acnes survive treatment, the team notes. And it won’t disrupt normal bacteria in healthy skin, which do not produce CAMP.
One approach Huang’s team plans to try is to develop monoclonal antibodies to CAMP that can be delivered locally, using microneedles, within the skin of people with acne. This would disrupt P. acnes-related inflammation without disturbing its better-behaved brethren elsewhere.