David L. Haviland, Ph.D. 1987, University or California, Riverside UT-Houston Institute of Molecular Medicine Center for Immunology and Autoimmune Diseases Contact Information

Research Interests: Immunology; complement; inflammation; chemotaxis; proinflammatory receptors; gene regulation; flow cytometry

Inflammatory processes direct the migration of polymorphonuclear neutrophils through the use of chemotactic factors that include the complement C5a anaphylatoxin, Interleukin-8, and N-formyl peptides. Specifically, N-formyl peptides are derived from bacterial degradation and possibly from mitochondrial proteins upon tissue damage. The infiltration of neutrophils and macrophages into tissues are thought to play an important role in the pathogenesis of many diseases such as adult respiratory distress syndrome (ARDS), inflammatory bowel disease, and rheumatoid arthritis. It is thought that through the degradation of bacteria or breakdown of mitochondria, N-formyl peptides are generated which in turn sequester neutrophils. Work in our laboratory centers around the expression, genetics, and regulation of the human N-formyl peptide receptor (fMLF-R). Although thought only to be expressed on myeloid cells, we have found the fMLF-R (as well as the C5a receptor) is expressed on non-myeloid cells such as liver parenchyma, cells of the central nervous system, and lung epithelium. What function and role in pathology the fMLF-R may play on these non-migrating tissues is unknown. This finding strongly suggests that the biological functions mediated by fMLF-R are likely to be more pleotropic and important than directing the migration of neutrophils.

A tutorial in this laboratory would involve the basic techniques of molecular biology, immunochemistry, tissue culture, flow cytometery.

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Biochemistry 32:4168-4174, 1993
J Immunol 154:1861-1869, 1995
J Exp Med 182:207-217, 1995
J Neuroimmunol 61:71-78, 1995

Program Affiliation:
Program in Immunology