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http://www.modernmed...ategoryId=44678
A new vaccine is being developed that sounds very promising.
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Troublemaker protein
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.
Sanofi-Pasteur says the joint project with Huang's team will "target the specific neutralisation of P. acnes factors in inflammation", though it has not revealed what the budget will be.
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.
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.
Sanofi-Pasteur says the joint project with Huang's team will "target the specific neutralisation of P. acnes factors in inflammation", though it has not revealed what the budget will be.
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.
