B
L. E. Bermudez, Wu, M., Miltner, E., and Inderlied, C. B.,
“Isolation of two subpopulations of Mycobacterium avium within human macrophages.”,
FEMS microbiology letters, vol. 178, no. 1, pp. 19-26, 1999.
L. E. Bermudez, Motamedi, N., Kolonoski, P., Chee, C., Baimukanova, G., Bildfell, R. J., Wang, G., Phan, L. Tam, and S Lowell, Y.,
“The efficacy of clarithromycin and the bicyclolide EDP-420 against Mycobacterium avium in a mouse model of pulmonary infection.”,
The Journal of infectious diseases, vol. 197, no. 11, pp. 1506-10, 2008.
L. E. Bermudez, Wu, M., and Young, L. S.,
“Interleukin-12-stimulated natural killer cells can activate human macrophages to inhibit growth of Mycobacterium avium.”,
Infection and immunity, vol. 63, no. 10, pp. 4099-104, 1995.
L. E. Bermudez, Kolonoski, P., Petrofsky, M., Wu, M., Inderlied, C. B., and Young, L. S.,
“Mefloquine, moxifloxacin, and ethambutol are a triple-drug alternative to macrolide-containing regimens for treatment of Mycobacterium avium disease.”,
The Journal of infectious diseases, vol. 187, no. 12, pp. 1977-80, 2003.
L. E. Bermudez, Young, L. S., and Gupta, S.,
“1,25 Dihydroxyvitamin D3-dependent inhibition of growth or killing of Mycobacterium avium complex in human macrophages is mediated by TNF and GM-CSF.”,
Cellular immunology, vol. 127, no. 2, pp. 432-41, 1990.
L. E. Bermudez, Danelishvili, L., and Early, J.,
“Mycobacteria and Macrophage Apoptosis: Complex Struggle for Survival.”,
Microbe Wash DC, vol. 1, no. 8, pp. 372-375, 2006.
L. E. Bermudez, Young, L. S., and Inderlied, C. B.,
“Rifabutin and sparfloxacin but not azithromycin inhibit binding of Mycobacterium avium complex to HT-29 intestinal mucosal cells.”,
Antimicrobial agents and chemotherapy, vol. 38, no. 5, pp. 1200-2, 1994.
L. E. Bermudez, Wu, M., Enkel, H., and Young, L. S.,
“Naturally occurring antibodies against Mycobacterium avium complex.”,
Annals of clinical and laboratory science, vol. 19, no. 6, pp. 435-43, 1989.
L. E. Bermudez, Parker, A., and Goodman, J. R.,
“Growth within macrophages increases the efficiency of Mycobacterium avium in invading other macrophages by a complement receptor-independent pathway.”,
Infection and immunity, vol. 65, no. 5, pp. 1916-25, 1997.
L. E. Bermudez, Wu, M., Petrofsky, M., and Young, L. S.,
“Interleukin-6 antagonizes tumor necrosis factor-mediated mycobacteriostatic and mycobactericidal activities in macrophages.”,
Infection and immunity, vol. 60, no. 10, pp. 4245-52, 1992.
L. E. Bermudez, Nash, K. A., Petrofsky, M., Young, L. S., and Inderlied, C. B.,
“Effect of ethambutol on emergence of clarithromycin-resistant Mycobacterium avium complex in the beige mouse model.”,
The Journal of infectious diseases, vol. 174, no. 6, pp. 1218-22, 1996.
L. E. Bermudez, Inderlied, C. B., Kolonoski, P., Petrofsky, M., and Young, L. S.,
“Clarithromycin, dapsone, and a combination of both used to treat or prevent disseminated Mycobacterium avium infection in beige mice.”,
Antimicrobial agents and chemotherapy, vol. 38, no. 12, pp. 2717-21, 1994.
L. E. Bermudez, Danelishvili, L., Babrack, L., and Pham, T.,
“Evidence for genes associated with the ability of Mycobacterium avium subsp. hominissuis to escape apoptotic macrophages.”,
Front Cell Infect Microbiol, vol. 5, p. 63, 2015.
L. E. Bermudez, Wu, M., and Young, L. S.,
“Intracellular killing of Mycobacterium avium complex by rifapentine and liposome-encapsulated amikacin.”,
The Journal of infectious diseases, vol. 156, no. 3, pp. 510-3, 1987.
L. E. Bermudez and Inderlied, C. B.,
“Effect of Mycobacterium avium infection on the influx, accumulation, and efflux of KRM-1648 by human macrophages.”,
Microbial drug resistance (Larchmont, N.Y.), vol. 3, no. 3, pp. 277-82, 1997.
L. E. Bermudez, Petrofsky, M., Inderlied, C. B., and Young, L. S.,
“Efficacy of azithromycin and rifabutin in preventing infection by Mycobacterium avium complex in beige mice.”,
The Journal of antimicrobial chemotherapy, vol. 36, no. 4, pp. 641-6, 1995.
L. E. Bermudez, Parker, A., and Petrofsky, M.,
“Apoptosis of Mycobacterium avium-infected macrophages is mediated by both tumour necrosis factor (TNF) and Fas, and involves the activation of caspases.”,
Clinical and experimental immunology, vol. 116, no. 1, pp. 94-9, 1999.