Medical News

Heat Shock Protein Prevents TB-Induced Arthritis in Animals

May 22, 2002

This article is part of The Body PRO's archive. Because it contains information that may no longer be accurate, this article should only be considered a historical document.

Administration of an immunogenic tuberculosis protein may ameliorate some of the side effects of TB infection, researchers report in International Immunopharmacology (2002;2;4:463-474).

"Adjuvant arthritis (AA) can be induced in Lewis rats by immunization with Mycobacterium tuberculosis (Mt) in oil," according to Dr. D. Agnello and colleagues at the Mario Negri Institute for Pharmacological Research in Milan. This condition was partially prevented by dosing with hsp10, a mycobacterial heat shock protein, Agnello and coauthors found. Multiple intranasal administrations of hsp10 strongly inhibited the inflammation and bone damage seen after exposure to incomplete Freund's adjuvant, they said. Other means of delivery failed to provide these benefits, although a marginal reduction in lymphocyte joint infiltration and bone resorption was seen. However, even seemingly ineffective treatment with hsp10 triggered the production of antibodies targeting the heat shock protein, study data showed. This humoral response was not accompanied by cell-mediated immune activity.

Levels of hsp-10-specific antibodies were correlated with the degree of AA suppression. "These antibodies mostly belonged to the IgG2a subtype, suggesting that immune deviation may play a role in the mechanism of disease suppression by hsp10," Agnello and colleagues concluded.

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Adapted from:
TB & Outbreaks Week
05.07.02; Michael Greer

This article was provided by CDC National Prevention Information Network. It is a part of the publication CDC HIV/Hepatitis/STD/TB Prevention News Update.


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