 | Shichun Lun, PhD Postdoctoral fellow |
| E-mail:slun1@jhmi.edu |
Research Interests
Mycobacterium tuberculosis has been a major killer throughout history, and claims about three million deaths worldwide every year. M. tuberculosis is able to persist in the human host for long periods of time even in the presence of active host immune response. During infection, latency, and reactivation, M. tuberculosis may use unique pathogenic mechanisms, which remain to be further defined. Some of the M. tuberculosis genes are not essential for in vitro growth, but are required for infection as shown by the mouse spleen model (Sassetti and Rubin, 2003) and mouse lung model (Lamichhane et al., 2005). My research interest is to characterize the function of the genes that are required for in vivo growth, elucidate the molecular mechanisms for M. tuberculosis virulence and explore the possibility of the candidate genes as potential genetic targets for new anti-tuberculosis drugs and gene products as vaccine candidates. In addition, M. tuberculosis is a slow growing microorganism that has the ability to enter a persistent or latent state during infection. Yet the explanation for why M. tuberculosis grows so slow has not been concretely defined. My secondary research interest is to study the cell division of mycobacteria.
Peer-reviewed publications:
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1. Nedeltchev, G. G., T. R. Raghunand, M. S. Jassal, S. Lun, Q. J. Cheng, and W. R. Bishai. 2009. Extrapulmonary dissemination of Mycobacterium bovis but not Mycobacterium tuberculosis in a bronchoscopic rabbit model of cavitary tuberculosis. Infect Immun 77:598-603.
2. Lun, S., and W. R. Bishai. 2007. Characterization of a novel cell wall-anchored protein with carboxylesterase activity required for virulence in Mycobacterium tuberculosis. J Biol Chem 282:18348-56.
3. Lun, S., G. Astrom, U. Magnusson, and K. Ostensson. 2007. Total and differential leucocyte counts and lymphocyte subpopulations in lymph, afferent and efferent to the supramammary lymph node, during endotoxin-induced bovine mastitis. Reprod Domest Anim 42:126-34.
4. Lun, S., and P. J. Willson. 2005. Putative mannose-specific phosphotransferase system component IID represses expression of suilysin in serotype 2 Streptococcus suis. Vet Microbiol 105:169-80.
5. Lun, S., and P. J. Willson. 2004. Expression of green fluorescent protein and its application in pathogenesis studies of serotype 2 Streptococcus suis. J Microbiol Methods 56:401-12.
6. Persson Waller, K., I. G. Colditz, S. Lun, and K. Ostensson. 2003. Cytokines in mammary lymph and milk during endotoxin-induced bovine mastitis. Res Vet Sci 74:31-6.
7. Lun, S., J. Perez-Casal, W. Connor, and P. J. Willson. 2003. Role of suilysin in pathogenesis of Streptococcus suis capsular serotype 2. Microb Pathog 34:27-37.
8. Lun S., Willson PJ. The resR gene, a member of two-component response regulators, is required for production of suilysin in Streptococcus suis type 2. (submitted for publication)
9. Lun S., Ostensson K, Magnusson U, Astrom Goran. Total and differential leukocyte counts and lymphocyte subpopulations in lymph, afferent and efferent to the supramammary lymph node, during endotoxin-induced mastitis in cows. (manuscript)
