First it was smallpox. Then polio. Now science has another of humanity鈥檚 scourges in its sights: acne.
Sanofi-Pasteur, the world鈥檚 biggest vaccine company, has with the University of California, San Diego, to develop 鈥渁n immunological approach to acne prevention and treatment鈥�.
Acne is no joke. 鈥淢ore than 85 per cent of teenagers and over 40 million people in the United States alone are suffering this disease鈥� and many adults have it too, says , head of the lab at the centre of the deal.
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Yet there is little effective treatment, says Huang. 鈥淭his collaboration will make our dreams of acne vaccines for the public come true earlier.鈥�
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 鈥� 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 鈥� partly by killing off its normal bacteria.
A major obstacle in acne research has been the lack of test animals 鈥� mice and guinea pigs don鈥檛 get spots. Huang鈥檚 lab got round that by injecting P. acnes into the skin of a mouse鈥檚 ear, causing inflammation. In 2008 they reported that mice given simple nasal-spray vaccines containing whole, dead P. acnes, or a , 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 from colonisation by nastier germs. A vaccine that encourages the body to indiscriminately attack P. acnes could cause worse trouble than acne.
Troublemaker protein
So the team tried a different approach: targeting , 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鈥檚 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鈥檛 disrupt normal bacteria in healthy skin, which do not produce CAMP.
Sanofi-Pasteur says the joint project with Huang鈥檚 team will 鈥渢arget the specific neutralisation of P. acnes factors in inflammation鈥�, though it has not revealed what the budget will be.
One approach Huang鈥檚 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.
