Dr. Shauna M. McGillivray
I have had a long-standing interest in understanding host-pathogen interactions, particularly between bacterial pathogens and the host innate immune system. In my lab, we use molecular and microbiological tools to identify and investigate the mechanism behind potential bacterial virulence genes. We primarily work with Bacillus anthracis, the causative agent of the deadly disease anthrax, as well as with the Staphylococcus aureus, the leading cause of skin and soft tissue infections. Currently, my lab studies a conserved intracellular bacterial protease called ClpXP and its role in virulence. Loss of ClpXP through genetic or pharmacological inhibition renders B. anthracis unable to survive in the host. One possible mechanism is due to increased susceptibility to antimicrobial peptides produced by the host innate immune system. The connection between ClpXP and bacterial defense against antimicrobial peptides is currently a major focus of investigation. My lab is also interested in the development of new antimicrobial agents. We are currently working in collaboration with Dr. Ken Keiler at Penn State University to investigate inhibiting trans-translation in S. aureus as a potential antibiotic target.
For more information, please refer to the following publications:
Franks SE, Ebrahimi C, Hollands A, Okumura CY, Aroian RV, Nizet V and McGillivray SM. Novel role for the yceGH tellurite resistance genes in the pathogenesis of Bacillus anthracis. (2014). Infect Immunity. 82 (3): 1132-40. Click here for PDF.
McGillivray SM, Tran DN, Ramadoss NS, Alumasa JN, Okumura CY, Sakoulas G, Vaughn MM, Zhang DX, Keiler KC and Nizet V. Pharmacological inhibition of the ClpXP protease increases bacterial susceptibility to host cathelicidin antimicrobial peptides and cell envelope-active antibiotics. (2012). Antimicrobial Agents and Chemotherapy. 56 (4): 1854-61. Click here for PDF.
McGillivray SM, Ebrahimi CM, Fisher N, Sabet M, Zhang DX, Chen Y, Haste NM, Aroian R, Gallo RL, Guiney DG, Friedlander AM, Koehler TM, and Nizet V. (2009). ClpX Protease Contributes to Antimicrobial Peptide Resistance and Virulence Phenotypes of Bacillus anthracis. Journal of Innate Immunity 1(5): 494-506. Click here for PDF.
This course is a general microbiology course geared towards junior/senior undergraduates. We cover a wide array of topics including microbial cell structure, genetics, diversity and ecology, host pathogen interactions and microbial diseases. This course includes a lab component emphasizing various lab techniques in microbiology including common stains, biochemical analysis, antimicrobial testing, and common lab techniques used in microbiology.
BIOL 40303/60403 Medical Microbiology
This course is geared towards senior undergraduates or graduate students and it focuses on advanced topics in medical microbiology including disease mechanisms of major human pathogens, the host response, and antibiotic development and resistance. Scientific approaches used to investigate these topics are emphasized. A major focus of this course is reading and discussion of the primary literature.
BIOL 30603 Cell Biology
This course is a required course for a major in biology and is geared towards sophomores. It focuses on basic structure and function of cellular components, molecular genetics, and important cell processes such as regulation of cell signaling, cell cycle, intracellular transport, etc. The course is team taught by 4 faculty including myself and Drs. Akkaraju, Chumley and Misamore.
Pre-Health Institute Responsibilties
I am Associate Director of the Pre-Health Institute and Associate Chair of the Health Professions Advisory Committee. We support students through academic and professional advising, interview preparation, letters of recommendation and pre-health related experiences and opportunities. For more information, please visit the Pre-Health Institute web page (http://www.prehealth.tcu.edu) or our Facebook page (https://www.facebook.com/TCUprehealth) where we post activities and student accomplishments throughout the year.