Publications:
1. Jeevan, A., Denkins, Y., Brown, E.L., and Kripke, M.L. 1991. Effects of UV radiation on infectious disease In:
Biologic Effects of Light. New York: Walter de Gruyter & Company. pp 83-96.
2. Jeevan, A., Evans, R., Brown, E.L., and Kripke, M.L. 1992. Effect of local ultraviolet irradiation on infections of
mice with Candida albicans, Mycobacterium bovis BCG, and Schistosoma mansoni. The Journal of Investigative
Dermatology 99:59-64.
3. Jeevan, A., Brown, E.L., and Kripke, M.L. 1995. UV and Infectious Diseases. In Photoimmunology. J. Krutmann,
and C. Elmets, editors. Cambridge: Blackwell Science. pp 153-163.
4. Brown, E.L., Rivas, J.M., Ullrich, S.E., Young, C.R., Norris, S.J., and Kripke, M.L. 1995. Modulation of immunity to
Borrelia burgdorferi by ultraviolet irradiation: differential effect on Th1 and Th2 immune responses. Eur J Immunol
25:3017-3022.
5. Pride, M.W., Brown, E.L., Stephens, L.C., Killion, J.J., Norris, S.J., and Kripke, M.L. 1998. Specific Th1 cell lines
that confer protective immunity against experimental Borrelia burgdorferi infection in mice. J Leukoc Biol 63:542-549.
6. Guo, B.P., Brown, E.L., Dorward, D.W., Rosenberg, L.C., and Höök, M. 1998. Decorin-binding adhesins from
Borrelia burgdorferi. Mol Microbiol 30:711-723.
7. Brown, E.L., Guo, B.P., O'Neal, P., and Höök, M. 1999. Adherence of Borrelia burgdorferi. Identification of critical
lysine residues in DbpA required for decorin binding. J Biol Chem 274:26272-26278.
8. Brown, E.L., Wooten, R.M., Johnson, B.J., Iozzo, R.V., Smith, A., Dolan, M.C., Guo, B.P., Weis, J.J., and Höök, M.
2001. Resistance to Lyme disease in decorin-deficient mice. J Clin Invest 107:845-852.
9. Brown, E.L., Ullrich, S.E., Pride, M., and Kripke, M.L. 2001. The effect of UV irradiation on infection of mice with
Borrelia burgdorferi. Photochem Photobiol 73:537-544.
10. Cooper, D., Pride, M.W., Brown, E.L., Risin, D., and Pellis, N.R. 2001. Suppression of antigen-specific
lymphocyte activation in modeled microgravity. In Vitro Cell Dev Biol Anim 37:63-65.
11. Lee, L.Y., Miyamoto, Y.J., McIntyre, B.W., Höök, M., McCrea, K.W., McDevitt, D., and Brown, E.L. 2002. The
Staphylococcus aureus Map protein is an immunomodulator that interferes with T cell-mediated responses. J Clin
Invest 110:1461-1471.
12. Pikas, D.S., Brown, E.L., Gurusiddappa, S., Lee, L.Y., Xu, Y., and Höök, M. 2003. Decorin-binding sites in the
adhesin DbpA from Borrelia burgdorferi: a synthetic peptide approach. J Biol Chem 278:30920-30926.
13. Willett, T.A., Meyer, A.L., Brown, E.L., and Huber, B.T. 2004. An effective second-generation outer surface
protein A-derived Lyme vaccine that eliminates a potentially autoreactive T cell epitope. Proc Natl Acad Sci U S A
101:1303-1308.
14. Xu, Y., Rivas, J.M., Brown, E.L., Liang, X., and Höök, M. 2004. Virulence potential of the Staphylococcal
adhesin CNA in experimental arthritis is determined by its affinity for collagen. J Infect Dis 189:2323-2333.
15. Lee, L.Y., Höök, M., Haviland, D., Wetsel, R.A., Yonter, E.O., Syribeys, P., Vernachio, J., and Brown, E.L. 2004. A
secreted Staphylococcus aureus protein inhibits complement activation. J Infect Dis 190:571-579.
16. Liang, F.T., Brown, E.L., Wang, T., Iozzo, R.V., and Fikrig, E. 2004. Protective niche for Borrelia burgdorferi to
evade humoral immunity. Am J Pathol 165:977-985.
17. Lee, L.Y., Liang, X., Hook, M., and Brown, E.L. 2004. Identification and characterization of the C3 binding
domain of the Staphylococcus aureus extracellular fibrinogen-binding protein (Efb). J Biol Chem 279:50710-50716.
18. Brown, E.L., Reisenbichler, E.S., Kim, J.-H., and Höök, M. 2005. Multicomponent Lyme vaccine: three is not a
crowd. Vaccine 23:3687-3696.
19. Ochoa, T.J., Brown, E.L., Guion, C.E., Chen, J.Z., McMahon, R.J., and Cleary, T.G. 2006. Effect of lactoferrin on
Enteroaggregative E. coli (EAEC). Biochem Cell Biol 84:369-376.
20. Jarvelainen, H., Puolakkainen, P., Pakkanen, S., Brown, E.L., Höök, M., Iozzo, R.V., Sage, E.H., and Wight, T.N.
2006. A role for decorin in cutaneous wound healing and angiogenesis. Wound Repair Regen 14:443-452.
21. Labandeira-Rey, M., Couzon, F., Boisset, S., Brown, E.L., Bes, M., Benito, Y., Barbu, E.M., Vazquez, V., Höök,
M., M., Etienne, J., et al. 2007. Staphylococcus aureus Panton-Valentine leukocidin causes necrotizing pneumonia.
Science 315:1082-1085.
22. Massey, R.C., Scriba, T.J., Brown, E.L., Phillips, R.E., and Sewell, A.K. 2007. Use of peptide-major
histocompatibility complex tetramer technology to study interactions between Staphylococcus aureus proteins and
human cells. Infect Immun 75:5711-5715.
23. Scriba, T.J., Sierro, S., Brown, E.L., Phillips, R.E., Sewell, A.K., and Massey, R.C. 2008. The S. aureus Eap
protein activates expression of proinflammatory cytokines. Infect Immun 76(5):2164-8.
24. Koo, H.L., Jiang, Z.D., Brown, E.L., Garcia, C., Qi, H., and DuPont, H.L. 2008. Coliform contamination of
vegetables obtained from popular restaurants in Guadalajara, Mexico, and Houston, Texas. Clin Infect Dis 47:218-221.
25. Huang, D.B., Brown, E.L., DuPont, H.L., Cerf, J., Carlin, L., Flores, J., Belkind-Gerson, J., Nataro, J.P., and
Okhuysen, P.C. . 2008. Seroprevalence of the enteroaggregative Escherichia coli virulence factor dispersin among
USA travellers to Cuernavaca, Mexico: a pilot study. J Med Microbiol 57:476-479.
26. Brown, E.L., Bowden, M.G., Bryson, R.S., Hulten, K.G., Bordt, A.S., Forbes, A., and Kaplan, S.L. 2009. The
Pediatric Antibody Response to Community-Acquired Staphylococcus aureus Infection is Directed to the Panton
Valentine Leukocidin. Clin Vaccine Immunol 16:139-141.
27. Brown, E.L., Dumitrescu, O., Thomas, D., Badiou, C., Koers, E.M., Choudhury, P., Vazquez, V., Etienne, J.,
Lina, G., Vandenesch, F., and Bowden, M.G. 2009. The Panton-Valentine leukocidin vaccine protects mice against
lung and skin infections caused by Staphylococcus aureus USA300. Clin Microbiol Infect 15:156-164.
28. Vigil K.J., Jiang Z.D., Chen J.J., Palumbo K.L., Galbadage T., Brown E.L., Yiang J. Koo H., DuPont M.W.,
Ericsson C., Adachi J.A., DuPont H.L. Coliform and Escherichia coli contamination of desserts served in public
restaurants from Guadalajara, Mexico, and Houston, Texas. 2009. Am J Trop Med Hyg. 80(4):606-608.
29. Brown, E.L., Xue, Q., Jiang, Z., DuPont, H.L. Pretreatment of epithelial cells with Rifaximin alters bacterial
attachment and internalization profiles. 2010. Antimicrobial Agents and Chemotherapy. 54:388-396.
30. Vandenesch F., Couzon F., Boisset S., Benito Y., Brown E.L., Lina G., Etienne J., and Bowden, M.G. The
Panton-Valentiine leukocidin is a virulence factor in a murine model of necrotizing pneumonia. 2010. J. Infect. Dis.
201:967-969.
31. Jiang Z.D., DuPont H.L., Brown E.L., Nandy R.K., Ramamurthy T., Sinha A., Ghosh S., Guin S., Gurleen K.,
Rodrigues S., Chen J.J., McKenzie R., Steffen R. Microbial Etiology of Travelers' Diarrhea in Mexico, Guatemala and
India Importance of Enterotoxigenic Bacteroides fragilis and Arcobacter Species. 2010. J. Clin. Microbiol.
48:1417-1419.
32. Espinoza, C., Fisher V., Jean W., Gaines B., Davis K, Wanger A., Brown E., Slomka J., Ostrosky-Zeichner L.
Prevalence and risk factors of methicillin-resistant Staphylococcus aureus colonization among critically ill
hospitalized patients in a tertiary care center in Houston, Texas: An active surveillance pilot project. 2011. Infect.
Cont. Hosp. Epidemiol. 32:93-95.
33. Shah, S.P., Grimes, C.Z., Brown, E., Hwang, L. Demographics, socio-behaviorl factors, and drug use patterns:
What matters in spontaneous HCV clearance. 2012. J. Med. Virol. 84:235-241.
34. Nichols, E.K., Nichols, J.S., Selwyn, B.J., Coello-Gomez, C., Parkerson, G.R., Brown, E.L., Day, R.S.
Implications of the WHO Child Growth Standards in rural Honduras. 2012. Public Health Nutr. 17:1-8.
35. Rudkin, J.K., Edwards, A.M., Bowden, M.G., Brown, E.L., Pozzi, C., Waters, E.M., Chan, W.C., Williams, P.,
O'Gara, J.P., Massey, R.C. Methicillin resistance reduces the virulence of healthcare-associated methicillin-resistant
Staphylococcus aureus by interfering with the agr quorum sensing system. 2012. J. Infect. Dis. IN PRESS.
36. Brown, E.L., NIshiyama, Y., Dunkle, J.W., Aggarwal, S., Planque, S., Watanabe, K., Smith, K.C., Bowden, M.G.,
Kaplan, S.L., Paul, S. Constitutive production of catalytic antibodies to a Staphylococcus aureus virulence factor and
effect of infection. 2012. J. Biol. Chem. IN PRESS.
| DoctorBrown.org This website provides research summaries of E.L. Brown's research projects, publications, lecture materials and scientific protocols. |
| Summary of Research Interests: Staphylococcal research: -Vaccine design -Mechanisms of disease -Translational medicine |
Staphylococcal disease:
S. aureus is an important human pathogen that causes a wide-range of disease states. S. aureus
colonizes the skin (primarily the anterior nasal vestibule) of approximately 30-50% (with 20-30%
persistently colonized) of the population without causing clinical disease symptoms.
Persistently colonized individuals are designated ‘carriers’.
Infections often result in severe and persistent joint damage, and mortality rates from this type
of infection are high. S. aureus is one of the most common causes of modern bacterial
infections, in part due to increasing resistance to antibiotics and the recent emergence of
infections caused by Community-Associated MRSA strains (CA-MRSA), which are now the
leading cause of bacterial infections not associated with hospitals. Although the CA-MRSA cases
are a growing concern, similar virulent isolates are still prevalent in hospitals and intensive care
units (hospital acquired infections), accounting for 40-70% of intensive care unit infections. In
2005, there were 94,360 invasive cases of MRSA in the United States, 18,650 resulted in death
(incidence rate of 31.8/100,000 persons). The incidence rate of other major bacterial pathogens is
lower (e.g., S. pneumoniae and H. influenzae, 14 to less than 1 per 100,000 people) (http://jama.
ama-assn.org/cgi/reprint/298/15/1763,
http://www.cdc.gov/ncidod/eid/vol12no12/pdfs/06-0505.pdf).
The changing epidemiology of infections caused by S. aureus also poses new challenges in the
implementation of preventive and treatment strategies. CA-MRSA infections have been
increasing steadily over the last several years worldwide, and the percentage of infections and
overall numbers of CA-MRSA cases have increased significantly in children from 2001-present.
Because of increased antibiotic resistance, antibiotic treatment options are diminishing,
necessitating the development of novel treatment modalities.
Our research interests encompass various inter-related areas associated with the development
of treatment modalities for S. aureus-related diseases:
i) Understanding the mechanisms of disease.
ii) Testing vaccine candidates.
iii) Developing novel treatment modalities based on purified and recombinant anti-
S. aureus-specific antibodies.
S. aureus is an important human pathogen that causes a wide-range of disease states. S. aureus
colonizes the skin (primarily the anterior nasal vestibule) of approximately 30-50% (with 20-30%
persistently colonized) of the population without causing clinical disease symptoms.
Persistently colonized individuals are designated ‘carriers’.
Infections often result in severe and persistent joint damage, and mortality rates from this type
of infection are high. S. aureus is one of the most common causes of modern bacterial
infections, in part due to increasing resistance to antibiotics and the recent emergence of
infections caused by Community-Associated MRSA strains (CA-MRSA), which are now the
leading cause of bacterial infections not associated with hospitals. Although the CA-MRSA cases
are a growing concern, similar virulent isolates are still prevalent in hospitals and intensive care
units (hospital acquired infections), accounting for 40-70% of intensive care unit infections. In
2005, there were 94,360 invasive cases of MRSA in the United States, 18,650 resulted in death
(incidence rate of 31.8/100,000 persons). The incidence rate of other major bacterial pathogens is
lower (e.g., S. pneumoniae and H. influenzae, 14 to less than 1 per 100,000 people) (http://jama.
ama-assn.org/cgi/reprint/298/15/1763,
http://www.cdc.gov/ncidod/eid/vol12no12/pdfs/06-0505.pdf).
The changing epidemiology of infections caused by S. aureus also poses new challenges in the
implementation of preventive and treatment strategies. CA-MRSA infections have been
increasing steadily over the last several years worldwide, and the percentage of infections and
overall numbers of CA-MRSA cases have increased significantly in children from 2001-present.
Because of increased antibiotic resistance, antibiotic treatment options are diminishing,
necessitating the development of novel treatment modalities.
Our research interests encompass various inter-related areas associated with the development
of treatment modalities for S. aureus-related diseases:
i) Understanding the mechanisms of disease.
ii) Testing vaccine candidates.
iii) Developing novel treatment modalities based on purified and recombinant anti-
S. aureus-specific antibodies.
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