W. Edward Swords
Assistant Professor of Microbiology and Immunology

B.S., 1988 (Biology) Auburn University
M.S., 1990 (Microbiology) Mississippi State University 
Ph.D., 1996 (Bacterial pathogenesis) University of Alabama - Birmingham

The major goals of my laboratory focus on understanding the interactions of Haemophilus influenzae with the host. H. influenzae is a commensal inhabitant of the airways of most healthy people, but is also an important opportunistic pathogen causing middle ear infections (otitis media) in children and respiratory infections in people with viral infections or damaged lungs. H. influenzae has a diverse population of glycolipids termed lipooligosaccharides (LOS) on its surface that are the target of innate host defenses. Our work showed that H. influenzae bacteria from opportunistic infections have very different LOS than those from benign carriage, suggesting that specific LOS forms mediate different outcomes in host/pathogen interactions. Ongoing work in the laboratory is defining how different LOS forms affect host responses. We work heavily in the areas of bacterial genetics, carbohydrate and lipid chemistry, and host cell biology and signal transduction.  

Recent Publications (selected):

Swords, W.E., P. Jones, and M. Apicella. 2003. The lipooligosaccharides of Haemophilus influenzae: an interesting array of characters. J Endotoxin Res, in press.

Swords, W. E., D. Chance, L. Cohn, J. Shao, M.A. Apicella, and A.L. Smith. 2002. Acylation of the lipooligosaccharide of Haemophilus influenzae and colonization: an htrB mutation diminishes the colonization of human airway epithelial cells. Infect Immun 70:4661-4668.

Swords, W. E., M.R. Ketterer, J. Shao, C.A. Campbell, J.N. Weiser, and M. A. Apicella. 2001. Binding of the non-typeable Haemophilus influenzae lipooligosaccharide to the PAF receptor initiates host cell signalling. Cell Microbiol 3:525-536.

Swords, W. E., B.A. Buscher, K. Ver Steeg, II, A. Preston, W.A. Nichols, J.N. Weiser, B.W. Gibson, and M.A. Apicella. 2000. Non-typeable Haemophilus influenzae adhere to and invade human bronchial epithelial cells via an interaction of lipooligosaccharide with the PAF receptor. Mol Microbiol 37:13-27.