Drs Toshiaki and Yuko Kawakami, working at the La Jolla Institute for Allergy & Immunology in California, have pinpointed the cellular defect that increases the likelihood of eczema sufferers, of developing eczema vaccinatum, a severe and potentially fatal reaction to the smallpox vaccine.
Drs Kawakami, a husband and wife scientific team, found that activity levels of Natural Killer (NK) cells played a vital role in the development of eczema vaccinatum in mice. The activity of the NK cells, which are disease fighting cells of the immune system, was significantly lower in the mice that developed eczema vaccinatum than in normal mice that also received the smallpox vaccine. Drs. Kawakami tested their theory by stimulating more NK cell activity in the eczema-infected mice. The higher activity led to the elimination of the eczema vaccinatum infection.
Since eczema affects as many as 17% of children in the US and since eczema vaccinatum carries a fatality rate of 5-10%, it is crucial that therapies that prevent or treat eczema vaccinatum are found lest the need for mass vaccination against smallpox arise in response, for example, to bioterrorism.
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Meanwhile, Michael Howell, assistant professor of peediatrics, and his colleagues at National Jewish Health, have shown that an antimicrobial agent, the synthetic compound CSA-13, can kill vaccinia virus in cell cultures and in mice; CSA-13 also stimulates cells to produce their own antimicrobial proteins.
CSA-13 is one of a class of compounds known as ceragenins, which were developed by Brigham Young University Professor Paul Savage to mimic antimicrobial proteins that occur naturally in the body. The ceragenins are smaller than antimicrobial proteins, and are not as vulnerable to degradation in the body. They have previously been shown to be effective against a variety of bacterial species.
Dr Howell and his colleagues had wanted to learn if CSA-13 could fight vaccinia virus infections and it demonstrated its effectiveness in three different tests.
When CSA-13 and vaccinia virus were directly incubated together, the CSA-13 killed more than 96% of the virus at a 25 micromolar concentration. When CSA-13 was added to cells infected with vaccinia, it both reduced vaccinia virus gene expression and allowed more of the infected cells to survive. Finally, the researchers infected immune-compromised mice with vaccinia virus, then applied CSA-13 onto their skin. The CSA-13 reduced the number of skin lesions caused by vaccinia virus.
Within their experiments, the researchers found that, in addition to directly killing the virus, CSA-13 also stimulated cells to produce their own antimicrobial proteins, LL-37 and HBD-3; they had previously shown that these antimicrobial proteins also exhibit antiviral activity against vaccinia virus.
'We knew from our plaque assays, that CSA-13 was directly killing the virus,' said Dr. Howell. 'But these experiments show that it also stimulates cells to produce their own antimicrobial proteins, which contribute to its disease-fighting capabilities. Our next step is to learn how CSA-13 stimulates cells' own innate immune defenses.'
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May/June 2009.
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