Department of Surgery - The Rumbaugh Lab
Contact Us:
Kendra Rumbaugh, Ph.D.
phone: 806-743-2460, ext. 264
fax: 806-743-2113
e-mail: kendra.rumbaugh@ttuhsc.edu
Related Link:
Texas Tech Women in Science:
http://www.ciser.ttu.edu/wis/default.aspx
Projects
Interkingdom signaling between P. aeruginosa Quorum Sensing Molecules and Host Cells
Quorum sensing (QS) is a cell density-dependent signaling process used by many bacteria to coordinate gene expression in a population. QS in Gram-negative bacteria is controlled by diffusible molecules called autoinducers (AI) that function as ligands for regulatable transcription factors. At least two separate QS systems exist in P. aeruginosa, the LasI/LasR and RhlI/RhlR systems. The ligands for LasR and RhlR are N-3-oxododecanoyl- and N-butyryl- homoserine lactones, or PAI-1 and PAI-2, respectively. Several studies indicate that bacterial autoinducers, and PAI-1 in particular, can also influence gene expression in host eukaryotic cells, a process we´ve termed interkingdom signaling. 
We hypothesize that this regulatory process involves autoinducer receptor molecules in the host cells, possibly transcription factors. We have shown that P. aeruginosa autoinducers can efficiently enter mammalian cells and modulate gene expression potentially through the interaction of nuclear hormone receptors. In addition we have also recently shown that the nematode C. elegans can sense bacterial autoinducers and use this sensory information to ‘learn’ to avoid pathogens.
Publications:
Jahoor A., Patel R., Bryan, A., Do C., Krier J., Watters C., Wahli W., Li, G., Williams S.C., Rumbaugh K.P. 2008. Peroxisome Proliferator Activated Receptors Mediate Host Cell Pro-inflammatory Responses to P. aeruginosa Autoinducer. 2008. J Bacteriol. Jan 4; [Epub ahead of print].
Rumbaugh, K.P. 2007. Convergence of Hormones and Autoinducers at the Host/Pathogen Interface. Anal Bioanal Chem. 387(2): 425-435.
Shiner, E.K., Terentyev, D., Bryan, A., Sennoune, S., Martinez-Zaguilan, R., Li, G., Gyorke, S., Williams, S.C. and Rumbaugh, K.P. 2006. Pseudomonas aeruginosa Autoinducer Modulates Host Cell Responses through Calcium Signaling. Cellular Microbiol. 8(10):1601-10.
Beale, E., Li, G., Tan, M.W., Rumbaugh, K.P. 2006. Caenorhabditis elegans Senses Bacterial Autoinducers. Appl Environ Microbiol. 72(7):5135-7.
Shiner, E.K., Rumbaugh, K. P., and S. C. Williams. 2005. Interkingdom Signaling: deciphering the language of homoserine lactones. FEMS Microbiol Rev. 29(5):935-47.
Shiner, E.K., S. Reddy, C. Timmons, G. Li, S.C. Williams, and K.P. Rumbaugh. 2004. Construction of a bacterial autoinducer detection system in mammalian cells. Biol Proced Online. 6:268-276.
Williams, S.C. Patterson, E. K., Carty, N.L., Griswold, J. A., Hamood, A. N. and K. P. Rumbaugh. 2004. Pseudomonas aeruginosa autoinducer enters and functions in mammalian cells. J. Bacteriol. 186(8): 2281-7.
Rumbaugh, K.P. 2004. The Language of Bacteria…and Just About Everything Else. The Scientist. 18(17):26-27.
Rumbaugh, K.P., A. N. Hamood and J. A. Griswold. 2004. Cytokine Induction by the P. aeruginosa quorum sensing system during thermal injury. J Surg Res. 116:137-144.
Rumbaugh, K. P., J. A. Griswold, and A. N. Hamood 2000. The role of quorum sensing in the in vivo virulence of Pseudomonas aeruginosa. Microbes Infect. 2:1-11.
Rumbaugh, K., J. A. Griswold, B. H. Iglewski, and A. N. Hamood. 1999. Contribution of quorum sensing to the virulence of Pseudomonas aeruginosa in burn wound infection. Infect. Immun. 67:5854-5862.
Rumbaugh, K., J. Griswold, and A. Hamood. 1999. Contribution of the regulatory gene lasR to the pathogenesis of Pseudomonas aeruginosa infection of burned mice. J Burn Care Rehabil. 20:42-49.
P. aeruginosa Pathogenesis and Biofilm Formation in Wounds
Infection with the Gram-negative pathogen Pseudomonas aeruginosa is one of the major causes of morbidity and mortality in severely burned patients, and the cause of debilitating chronic infections in diabetic patients. P. aeruginosa relies on an arsenal of cell-associated and secreted virulence factors to colonize and infect its host, and it persists and invades the immune system by building biofilms. We have recently shown that P. aeruginosa forms biofilm in burn wounds, specifically surrounding blood vessels and adipocytes. Currently, we are focusing on characterizing the biofilms formed in chronic diabetic wounds.
Publications:
Rumbaugh, K.P. 2007. Pseudomonas aeruginosa forms Biofilms in Acute Infection Independently of Cell-to-Cell Signaling. Infect Immun. 75(8)p. 3715-21.
Haynes, A., Ruda, F., Oliver, J., Hamood. A.N., Griswold, J.A., Park, P.W., Rumbaugh, K.P. 2005. Syndecan-1 Shedding Contributes to Pseudomonas aeruginosa Sepsis. Infect Immun. 73(12):7914-21.
Haynes, A., Rumbaugh, K. P., Park, W. P., Hamood, A. N., Griswold, J. A. 2005. Protamine sulfate reduces the susceptibility of thermally injured mice to Pseudomonas aeruginosa infection. J. Surg. Res. 123: 109-117.
Fogle M. R., Griswold J. A., Oliver J. W., Hamood A. N. 2002. Anti-ETA IgG neutralizes the effects of Pseudomonas aeruginosa exotoxin A. J Surg Res. 106:86-98.
Rumbaugh, K. P., J. A. Colmer, J. A. Griswold, and A. N. Hamood 2001. The effects of infection of thermal injury by Pseudomonas aeruginosa PAO1 on the murine cytokine response. Cytokine. 16:160-168.
Rumbaugh, K., J. A. Griswold, and A. N. Hamood. 1999. Pseudomonas aeruginosa strains obtained from patients with tracheal, urinary tract, and wound infection: variations in virulence factors and virulence gene. J. Hosp. Infect. 43:211-218.
Rumbaugh, K., A. N. Hamood, and J. A. Griswold. 1999. Analysis of Pseudomonas aeruginosa clinical isolates for possible variations within the virulence genes exotoxin A and exoenzyme S. J Surg Res. 82:95-105.
