Ian J. Glomski
- Former Assistant Professor, Unaffiliated
- Phone: 434-924-2812
- Email: firstname.lastname@example.org
- Website: http://www.medicine.virginia.edu/basic-science/departments/microbiology-immunology-and-cancer-biology/mic-labs/glomski-lab
Elucidating the molecular mechanisms of B. anthracis pathogenesis; detection and prevention of anthrax.
Bacillus anthracis is a spore forming Gram positive bacterial pathogen that causes the disease anthrax. Infection can occur via three different routes, gastro-intestinal, cutaneous, or inhalational. Bacterial spores introduced by each route have different levels of virulence and different hallmarks of disease. Systemic disease is associated with both toxemia and sepcemia; where two secreted toxins, lethal toxin and edema toxin, are responsible for toxemia, and encapsulation, which reduces phagocytosis by host defense cells, is responsible for sepcemia.
B. anthracis gained public notoriety when it was used as a bioweapon in the United States postal system in the autumn of 2001, but it has long been feared for its devastation of livestock herds and as an agent of zoonotic infectious disease from domesticated animals. Thanks to a highly effective animal vaccine anthrax is very rare in the developed world. Yet because anthrax was considered a “beaten” disease, thanks to this efficacious veterinary vaccine, relatively little attention has been paid to the basic molecular mechanisms of how this bacterium causes disease. Thus, surprisingly little is known about how B. anthracis causes pathology (or pathogenesis) in an infected host.
Our laboratory’s goal is to elucidate the molecular mechanisms of B. anthracis pathogenesis and use this knowledge to guide research towards better means of detection and prevention of anthrax. We advance these goals by using techniques derived from bacterial genetics, molecular biology, biochemistry, immunology, and tissue culture and animal models of disease. Our past projects have focused on: 1) innate immune responses to B. anthracis spores, 2) the mechanisms of immune protection granted by vaccination with an experimental vaccine, and 3) the development of real-time small animal models of infection using bioluminescent bacteria that can be detected within infected animals (see photos and references). Future projects will expand upon these themes, but also include greater concentration on revealing the contribution of bacterial factors in B. anthracis pathogenesis. Images of mice infected with an aerosol of bioluminescent Bacillus anthracis at the indicated times.
- Weiner Z, Boyer A, Gallegos-Candela M, Cardani A, Barr J, Glomski I. Debridement increases survival in a mouse model of subcutaneous anthrax. PloS one. 2012;7(2): e30201. PMID: 22393351 | PMCID: PMC3290625
- Weiner Z, Glomski I. Updating perspectives on the initiation of Bacillus anthracis growth and dissemination through its host. Infection and immunity. 2012;80(5): 1626-33. PMID: 22354031 | PMCID: PMC3347428
- Crawford M, Lowe D, Fisher D, Stibitz S, Plaut R, Beaber J, Zemansky J, Mehrad B, Glomski I, Strieter R, Hughes M. Identification of the bacterial protein FtsX as a unique target of chemokine-mediated antimicrobial activity against Bacillus anthracis. Proceedings of the National Academy of Sciences of the United States of America. 2011;108(41): 17159-64. PMID: 21949405 | PMCID: PMC3193227
- Drygiannakis I, Ernst P, Lowe D, Glomski I. Immunological alterations mediated by adenosine during host-microbial interactions. Immunologic research. 2011;50(1): 69-77. PMID: 21479929 | PMCID: PMC3361322
- Dumetz F, Jouvion G, Khun H, Glomski I, Corre J, Rougeaux C, Tang W, Mock M, Huerre M, Goossens P. Noninvasive imaging technologies reveal edema toxin as a key virulence factor in anthrax. The American journal of pathology. 2011;178(6): 2523-35. PMID: 21641378 | PMCID: PMC3124019
- Klimecka M, Chruszcz M, Font J, Skarina T, Shumilin I, Onopryienko O, Porebski P, Cymborowski M, Zimmerman M, Hasseman J, Glomski I, Lebioda L, Savchenko A, Edwards A, Minor W. Structural analysis of a putative aminoglycoside N-acetyltransferase from Bacillus anthracis. Journal of molecular biology. 2011;410(3): 411-23. PMID: 21601576 | PMCID: PMC3131501
- Crawford M, Burdick M, Glomski I, Boyer A, Barr J, Mehrad B, Strieter R, Hughes M. Interferon-inducible CXC chemokines directly contribute to host defense against inhalational anthrax in a murine model of infection. PLoS pathogens. 2010;6(11): e1001199. PMID: 21124994 | PMCID: PMC2987825
- Fedhila S, Buisson C, Dussurget O, Serror P, Glomski I, Liehl P, Lereclus D, Nielsen-LeRoux C. Comparative analysis of the virulence of invertebrate and mammalian pathogenic bacteria in the oral insect infection model Galleria mellonella. Journal of invertebrate pathology. 2009;103(1): 24-9. PMID: 19800349
- Glomski I, Corre J, Mock M, Goossens P. Cutting Edge: IFN-gamma-producing CD4 T lymphocytes mediate spore-induced immunity to capsulated Bacillus anthracis. Journal of immunology (Baltimore, Md. : 1950). 2007;178(5): 2646-50. PMID: 17312104
- Glomski I, Corre J, Mock M, Goossens P. Noncapsulated toxinogenic Bacillus anthracis presents a specific growth and dissemination pattern in naive and protective antigen-immune mice. Infection and immunity. 2007;75(10): 4754-61. PMID: 17635863 | PMCID: PMC2044546
- Glomski I, Piris-Gimenez A, Huerre M, Mock M, Goossens P. Primary involvement of pharynx and peyer's patch in inhalational and intestinal anthrax. PLoS pathogens. 2007;3(6): e76. PMID: 17542645 | PMCID: PMC1885272
- Glomski I, Fritz J, Keppler S, Balloy V, Chignard M, Mock M, Goossens P. Murine splenocytes produce inflammatory cytokines in a MyD88-dependent response to Bacillus anthracis spores. Cellular microbiology. 2006;9(2): 502-13. PMID: 16978234