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ORIGINAL RESEARCH ARTICLE

A BRIEF COMMUNICATION

Collagen Fragments Modulate Innate Immunity

Amelia H. Thomas^*, Elazer R. Edelman^,, and Collin M. Stultz^*,,,||,1

^* The Computer Science and Artificial Intelligence Laboratory, Cambridge, Massachusetts 02139; and The Harvard-MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139; and The Department of Medicine, Brigham and Women’s Hospital, Boston, Massachusetts 02115; and The Division of Cardiovascular Disease, Brigham & Women’s Hospital, Boston, Massachusetts 02115; and ^|| The Department of Electrical Engineering and Computer Science, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139

To whom requests for reprints should be addressed at ¹ MIT, The Stata Center, 32–310, 32 Vassar Street, Cambridge, MA 02139. E-mail: cmstultz{at}mit.edu

Activation of the innate immune response in diseases such as rheumatoid arthritis and atherosclerosis leads to the production of proinflammatory cytokines that can promote collagenolysis. While a number of studies suggest that inflammation plays a major role in initiating collagen degradation, the effect of collagen and collagen-degradation fragments on the inflammatory response is not well understood. We now demonstrate that different collagen fragments can either augment or suppress IL-1ß production from human peripheral-blood monocytes. These data have wide-ranging implications for how amino acid variation in collagen affects disease and suggest that collagen degradation leads to the production of peptides that can modulate inflammation.

Key Words: collagen • cytokines • inflammation • interleukin-1