Microbiology and Immunology
Faculty research interests in the area of microbiology and immunology include viral pathogenesis (McQueen Lab), fungal pathogenesis (Park Lab), innate mucosal immunity (Porter Lab), environmental microbiology (Salmassi Lab), and applied microbiology and biotechnology (Xu Lab). An asterisk following a name in a publication citation indicates a student coauthor.
|Contact: Nancy McQueen, Ph.D.|
Office: ASCL 354, ext: 3-2036
Laboratory: ASCL 331, ext: 3-6265
|Cultures of kidney cells (MDCK) expressing the mutant M protein from the F1-R variant of Sendai virus. The mutant protein disrupts the microtubule network causing slow growth, restricted mitosis, and an increase to 40 times the normal cell size.|
Our lab studies the pathogenesis of Sendai virus, an RNA virus that causes a respiratory tract infection in rodents that is similar to influenza, parainfluenza, and respiratory syncytial virus infections of man. Information gained from studying Sendai virus may shed light on how these viral respiratory pathogens of man cause infection. Our studies have focused on a mutant virus, F1-R, which causes a systemic infection rather than the normal Sendai virus infection that is localized in the respiratory tract. To identify mutations and resulting phenotypic changes that correlate with the ability of F1-R to cause a systemic infection, we use reverse genetics to make viruses with defined mutations. We then test the reverse genetics viruses in both tissue culture and mice to assess changes in viral pathogenesis. Changes in the pathogenesis can then be attributed to the viral mutations that we have made.
|McQueen, N.L., Tashiro, M and Seto, J.T. 2007. Molecular biology of the pathogenesis of Sendai virus host range mutant, F1-R. In Influenza Viruses - Facts and Prospectives, M.F.G. Schmidt (ed). Grosse Verlag Berlin., pgs 85-87.|
|Hou, X., Suquilanda, E., Zeledon, A., Kacsinta, A.*, Moore, A., Seto, J., and McQueen, N.L. 2005. Mutations in Sendai virus variant F1-R that correlate with plaque formation in the absence of trypsin. Medical Microbiology and Immunology 194: 129-136.|
|Tashiro, M., McQueen, N.L., and Seto, J.T. 1999. Determinants of organ tropism of Sendai virus. Frontiers in Bioscience 4: 642-645.|
|Okada, H., Seto, J.T., McQueen, N.L., Klenk, H.-D., Rott, R., and Tashiro, M. 1998. Determinants of pantropism in the F1-R mutant of Sendai virus: specific mutations involved are in the F and M genes. Archives of Virology 143: 2343-2352.|
|Tashiro, M., McQueen, N.L., Seto, J.T., Klenk, H.-D., and Rott, R. 1996. Involvement of the mutated M protein in altered budding polarity of a pantropic mutant, F1-R, of Sendai virus. Journal of Virology 70: 5990-5997.|
|Contact: Hyunsook Park, Ph.D.|
Office: ASCL 353, ext: 3-2060
Laboratory: ASCL 348, ext: 3-2035
|Confocal microscopy of the yeast C. albicans grown with oral epithelial cell. Germ tube (on the right) penetrates into the mammalian cell.|
Our research program focuses on host-pathogen interactions in infectious disease. In particular, we have focused on the pathogenic mechanisms of the fungus Candida albicans during the initiation of oropharyngeal candidiasis. We are identifying key virulence factors governing the early stage of oral candidiasis using a transcriptional profiling analysis and gene disruption approach.
|Park, H., Liu, Y., Solis, N., Spotkov, J., Hamaker, J., Blankenship, J.R., Yeaman, M.R., Mitchell, A.P., Liu, H., and Filler, S.G. 2009. Transcriptional responses of Candida albicans to epithelial and endothelial cells. Eukaryotic Cell (in press).|
|Gank, K.D., Yeaman, M.R., Kojima, S., Yount, N.Y., Park, H., Edwards, Jr., J.E., Filler, S.G., and Fu, Y. 2008. SSD1 is integral to host defense peptide resistance in Candida albicans. Eukaryotic Cell, May 30.|
|Barker, K.S., Park, H., Phan, Q.-T., Xu, L., Homayouni, R., Liu, T.T., Rogers, P.D., and Filler, S.G. 2008. Transcriptome profile of the vascular endothelial cell response to Candida albicans. Journal of Infectious Diseases 198: 193-202.|
|Martinez-Lopez, R., Park, H., Myers, C.L., Gil, C., and Filler, S.G. 2006. Candida albicans Ecm33p is important for normal cell wall architecture and interactions with endothelial and oral epithelial cells. Eukaryotic Cell 5: 140-147.|
|Park, H., Myers, C.L., Sheppard, D.C., Phan, Q.T., Sanchez, A.A., Edwards, Jr., J.E. and Filler, S.G. 2005. Role of the fungal ras-protein kinase A pathway in governing epithelial cell interactions during oropharyngeal candidiasis. Cellular Microbiology 7: 499-510.|
|Contact: Edith Porter, M.D.|
Office: ASCL 355, ext: 3-6353
Laboratory: ASCL 333, ext: 3-2079
|Transmission electron microscopy, 10,000-fold magnification, of Pseudomonas aeruginosa showing ultrastructural changes of the cell wall after treatment with the free fatty acid docosahexaenoic acid and the antimicrobial polypeptide lysozyme.|
Our research focuses on mucosal innate immunity, specifically, antimicrobial effector molecules that directly act on and kill bacterial pathogens. A great deal of our work has targeted the activity and regulation of the antimicrobial peptide human defensin 5 in the intestinal and genital tract and the response of Paneth cells, specialized defense cells in the small intestine, to infection with Salmonella. Recently, we have begun to explore role of host-derived antimicrobial lipids, in particular cholesteryl esters, in the mucosal defense of the respiratory and genital tract.
|Rodriguez, N.R.*, Eloi, M.D.*, Huynh, A.*, Dominguez, T.*, Cheung Lam, A.H.*, Carcamo-Molina, D.*, Naser, Z.*, Desharnais, R., Salzman, N.H., and Porter, E. 2012. Expansion of Paneth Cell Population in Response to Enteric Salmonella Infection. Infection and Immunity 80: 266-275.|
|Spencer, J.D., Hains, D.S., Porter, E., Bevins C.L., Dirosario J., Becknell B., Wang H., and Schwaderer A.L. 2012. Human alpha defensin 5 expression in the human kidney and urinary tract. PLoS One 7: e31712.|
|Lee, J.T., Jansen, M.*, Yilma, A.N.*, Nguyen, A.*, Desharnais, R., and Porter, E. 2010. Antimicrobial lipids: novel innate defense molecules are elevated in sinus secretions of patients with chronic rhinosinusitis. American Journal of Rhinology & Allergy 24: 99-104.|
|Martinez, J.G.*, Waldon, M.*, Huang, Q.*, Alvarez, S.*, Oren, A., Sandoval, N.*, Du, M., Zhou, F., Zenz, A., Lohner, K., Desharnais, R., and Porter, E. 2009. Membrane-targeted synergistic activity of docosahexaenoic acid and lysozyme against P. aeruginosa. Biochemical Journal 419: 193-200.|
|Do, T.Q., Moshkani, S.*, Castillo, P.*, Anunta, S.*, Pogosyan, A.*, Cheung, A.*, Marbois, B., Faull, K.F., Ernst, W., Chiang, S.M., Fujii, G., Clarke, C.F., Foster, K., and Porter, E. 2008. Lipids including cholesteryl linoleate and cholesteryl arachidonate contribute to the inherent antibacterial activity of human nasal fluid. Journal of Immunology 181: 4177-4187.|
|Contact: Tina Salmassi, Ph.D.|
Office: ASCL 315, ext: 3-2065
Laboratory: ASCL 327, ext: 3-2083
|Arsenite oxidizing bacterium (Agrobacterium albertimagni strain AOL15) isolated from the surface of aquatic plants at Hot Creek, California.|
Our laboratory is interested in the interactions between microbes and the environment. We use classical microbiology and molecular biology techniques to study the diversity of bacteria in a variety of environments such as soils, natural waters, plant surfaces, and the hindgut of termites. By observing bacteria both in their natural niches and under controlled laboratory conditions, we hope to better understand the chemistry carried out by these microscopic organisms and their role in the biogeochemical cycling of the elements.
|Pech, H.*, Vazquez, M.*, Van Buren, J.*, Shi, L., Salmassi, T.M., Pasek, M.A., and Foster, K. 2011. Elucidating the redox cycle of reduced phosphorus using ion chromatography. Journal of Chromatographic Science 59: 573-581.|
|Pech, H.*, Henry, A.*, Khachikian, C.S., Salmassi, T.M. Hanrahan, G., and Foster, K.L. 2009. Detection of geothermal phosphite using high-performance liquid chromatography. Environmental Science and Technology 43: 7671-7675.|
|Barco, R.A.*, Patil, D.G.*, Xu, W., Ke, L., Khachikian, C.S., Hanrahan, G., and Salmassi, T.M. 2006. The development of iodide-based methods for batch and on-line determinations of phosphite in aqueous samples. Talanta 69: 1292-1299.|
|Salmassi, T.M., Walker, J.J., Newman, D.K., Leadbetter, J.R., Pace, N.R., and Hering, J.G. 2006. Community and cultivation analysis of arsenite oxidizing biofilms at Hot Creek. Environmental Microbiology 8: 50-59.|
|Hanrahan, G., Salmassi, T.M., Khachikian, C.S., and Foster, K.L. 2005. Reduced inorganic phosphorus in the natural environment: significance, speciation and determination. Talanta 66: 435-444.|
|Contact: Howard Xu, Ph.D.|
Office: ASCL 356, ext: 3-2188
Laboratory: ASCL 337, ext: 3-2040
|Determination of the lowest concentration of an antibacterial compound to totally inhibit the growth of Pseudomonas aeruginosa (yellow color). Compounds were serially (2 fold) diluted from top to bottom wells.|
Our long-term objective is to contribute in the fight against bacterial pathogens through the discovery of novel antibiotic therapeutics, the development of rapid pathogen detection technologies, and molecular characterization of bacterial pathogens. This objective will be achieved by employing several modern, novel and complimentary approaches: bacterial functional genomics, microbial physiology, biochemistry, molecular biology, novel assay development, high-throughput screening, and clinical microbiology. Critical to the success of various research projects are the ongoing collaborations with our colleagues on campus, from UCLA, Los Angeles County USC Medical Center, Indiana University, University of Michigan, National Laboratories, and Canada's National Research Council.
|Meng, J.*, Kanzaki, G.*, Meas, D.*, Lam, C.K.*, Crummer, H.*, Tain, J.*, and Xu, H.H. 2012. A genome-wide inducible phenotypic screen identifies antisense RNA constructs silencing Escherichia coli essential genes. FEMS Microbiology Letters 329: 45-53.|
|Yuan, H., Chai, S.C., Lam, C.K.*, Xu, H.H., and Ye, Q.Z. 2011. Two methionine aminopeptidases from Acinetobacter baumannii are functional enzymes. Bioorganic & Medicinal Chemistry Letters 21: 3395-3398.|
|Golanbar, G.D.*, Lam, C.K.*, Chu, Y.M.*, Cueva, C.*, Tan, S.W.*, Silva. I.*, and Xu. H.H. 2011. Phenotypic and molecular characterization of Acinetobacter clinical isolates obtained from inmates of California correctional facilities. Journal of Clinical Microbiology 49: 2121-2131.|
|Xu, H.H., Trawick, J.D., Haselbeck, R.J., Forsyth, R.A., Yamamoto, R.T., Archer, R., Patterson, J., Allen, M., Froelich, J.M., Taylor, I., Nakaji, D., Maile, R., G. C., K., Pilcher, M., Brown-Driver, V., McCarthy, M., Files, A., Robbins, D., King, P., Sillaots, S., Malone, C., Zamudio, C.S., Roemer, T., Wang, L., Youngman, P.J., and Wall, D. 2010. Staphylococcus aureus TargetArray: Comprehensive differential essential gene expression as a mechanistic tool to profile antibacterials. Antimicrobial Agents and Chemotherapy. 54: 3659-3670.|
|Valentine, S.C.*, Contreras, D.*, Tan, S.*, Real, L.J.*, Chu, S., and Xu, H.H. 2008. Phenotypic and molecular characterization of Acinetobacter baumannii clinical isolates from nosocomical outbreaks in Los Angeles County, California. Journal of Clinical Microbiology 46: 2499-2507.|
Note: ASCL = Wallis Annenberg Integrated Science Complex-Wing A (La Kretz Hall). When calling from off-campus, the area code and prefix for all telephone extensions is (323) 34X-XXXX.