Protective effects of hsp70 in inflammation View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1994-11

AUTHORS

M. R. Jacquier-Sarlin, K. Fuller, A. T. Dinh-Xuan, M. -J. Richard, B. S. Polla

ABSTRACT

Inflammation results from the recruitment to a given tissue or organ and the activation of leucocytes, among which the monocytes-macrophages play a major role. These phagocytic cells produce high levels of reactive oxygen species (ROS) as well as cytokines. Whereas both ROS and cytokines have the potential to regulate the expression of heat shock (HS)/stress proteins (HSP), it appears that these proteins in turn have the ability to protect cells and tissues from the deleterious effects of inflammation. The mechanisms by which such protection occurs include prevention of ROS-induced DNA strand breaks and lipid peroxidation as well as protection from mitochondrial structure and function. In vivo, HS protects organs against a number of lesions associated with the increased production of ROS and/or cytokines. In an animal model for adult respiratory distress syndrome, an acute pulmonary inflammatory condition, HS completely prevented mortality. HSP (hsp70 in particular) may also exert protective effects in the immune system by contributing to the processing and presentation of bacterial and tumoral antigens. The analysis of the expression of hsp70 may prove of diagnostic and prognostic value in inflammatory conditions and therapeutical applications are being considered. More... »

PAGES

1031-1038

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/bf01923458

DOI

http://dx.doi.org/10.1007/bf01923458

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1051703907

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/7988662


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