Adeline (Lynn) Hajjar, D.V.M., Ph.D.
Research Associate Professor, Immunology

Department of Immunology
University of Washington
Office: H-451 HSC, Box 357650
1959 NE Pacific Street
Seattle, WA 98195-7330
Tel: 206.221-2817
Fax: 206.543-1013
Email: hajjar@u.washington.edu

Lynn Hajjar obtained her DVM in 1988 from the University of Illinois. She then continued her graduate studies in the laboratory of Maxine Linial at the Fred Hutchinson Cancer Research Center in Seattle and obtained a PhD in 1995 from the University of Washington. She also completed a residency in Laboratory Animal Medicine in 1992 at the University of Washington. She had one year of postdoctoral training in the laboratory of Julie Overbaugh (now at FHCRC) before joining Chris Wilson’s laboratory where she is currently a Research Assistant Professor.

Toll-like receptors (TLR) are pattern-recognition receptors that recognize molecular patterns expressed by microbial organisms. This family of receptors mediates early innate responses. We are interested in understanding how specificity is achieved in this “non-antigen specific” response. One organism of interest is Pseudomonas aeruginosa (PA), a Gram-negative bacterium that infects individuals with cystic fibrosis. Mice deficient in MyD88, an adapter protein required for signaling downstream of most TLRs, are highly susceptible to PA infection. PA expresses ligands that are recognized by TLR2 (lipoproteins), TLR4 (lipopolysaccharide, LPS), TLR5 (flagellin), and TLR9 (DNA). By using various combinations of TLR knockout mice and mutant bacteria, we are studying the contribution of each of these TLRs to the response to PA. In other studies, we have also demonstrated that mouse and human TLR4 differ in their recognition of PA LPS. Therefore, we are generating humanized TLR4 mice to examine the consequences of this differential recognition in vivo.

Representative publications:

Hajjar AM*, Ernst RK*, Tsai JH, Wilson CB**, Miller SI**. Human Toll-like receptor 4 recognizes host-specific LPS modifications. Nature Immunol 3:354-359, 2002.

Ernst RK, Hajjar AM, Tsai JH, Moskowitz SM, Wilson CB, Miller SI. Pseudomonas aeruginosa lipid A diversity and its recognition by Toll-like receptor 4. J Endotoxin Res 9:395-400, 2003.

Skerrett SJ, Liggitt HD, Hajjar AM, Wilson CB. Cutting edge: Myeloid differentiation factor 88 is essential for pulmonary host defense against Pseudomonas aeruginosa but not Staphylococcus aureus. J Immunol 172:3377-81, 2004.

Darveau RP, Pham TT, Lemley K, Reife RA, Bainbridge BW, Coats SR, Howald WN, Way SS, Hajjar AM. Porphyromonas gingivalis lipopolysaccharide contains multiple lipid A species that functionally interact with both toll-like receptors 2 and 4. Infect Immun 72:5041–5051, 2004.

Hajjar AM, Harowicz H, Liggitt HD, Fink PJ, Wilson CB, Skerrett SJ. An essential role for non-bone marrow-derived cells in control of Pseudomonas aeruginosa pneumonia. Am J Respir Cell Mol Biol 33:470-5, 2005.

*contributed equally **share senior authorship

Updated August 2006