I graduated from Emory University in 1987 and then spent 2 years as a research assistant in the Department of Pediatric Biochemistry at Emory Hospital. My research experience at Emory prompted me to study animal medicine and I received the D.V.M., cum laude from the University of GA in 1993. At UAB I have received excellent training in laboratory animal medicine, and molecular and Cellular Pathology (Ph.D. December 1998; mentor, Dr. Lindsey). My dissertation research has produced a number of important advances in understanding pulmonary antimycoplasmal defenses applicable to human disease. This SERCA provides the ideal setting for my desired maturation into an independent comparative medicine scientist. Mycoplasma pneumoniae is a leading cause of pneumonia and extrapulmonary disease in humans. C57BL mice are highly resistant and C3H mice are highly susceptible to Mycoplasma pulmonis and are excellent models of the human disease. I have shown that the alveolar macrophage (AM) is the key cell in resistance of C57BL mice, and surfactant protein A (SP-A) mediates the killing of mycoplasmas by C57BL AMs in vitro through the production of reactive oxygen-nitrogen species. Furthermore, my results suggest for the first time that AM nitric oxide derived species, but not reactive oxygen species, are essential for killing mycoplasmas in vivo and in vitro.
My aims for the 01-03 years are: (1) Determine the molecular mechanism(s) responsible for SP-A mediate mycoplasmal killing by C57BL AMs in vivo and in vitro, and (2) Identify the mechanism responsible for the defect in SP-A mediated killing by susceptible C3H AMs in vivo and in vitro. My tentative plan for the 04-05 years is to investigate the mechanism by which reactive species damage and effect killing of mycoplasmas, and the pathophysiologic sequelae of mycoplasmal injury to alveolar epithelium in vivo. My career will emphasize the development of models and the investigation of immunologic mechanisms for resistance/susceptibility to bacterial pneumonias, utilizing transgenic and other methodologies. Thus, I plan to perform experiments in vivo, to show the relevance of my findings in human disease, and in vitro to identify the basic mechanisms. This SERCA with Dr. Matalon (lung physiology, biochemistry) as advisor and Drs. Lindsey (mycoplasmal diseases, lung defenses) and Wood (molecular genetics, transgenics) as co-advisors provides a unique and extremely stimulating environment, ideal for my desired maturation into an independent scientist focused on the development of models for pneumonic processes.
| Hickman-Davis, Judy M; McNicholas-Bevensee, Carmel; Davis, Ian C et al. (2006) Reactive species mediate inhibition of alveolar type II sodium transport during mycoplasma infection. Am J Respir Crit Care Med 173:334-44 |
| Hickman-Davis, Judy M; Gibbs-Erwin, Julie; Lindsey, J Russell et al. (2004) Role of surfactant protein-A in nitric oxide production and mycoplasma killing in congenic C57BL/6 mice. Am J Respir Cell Mol Biol 30:319-25 |
| O'Reilly, Philip J; Hickman-Davis, Judy M; Davis, Ian C et al. (2003) Hyperoxia impairs antibacterial function of macrophages through effects on actin. Am J Respir Cell Mol Biol 28:443-50 |
| Hickman-Davis, Judy M; O'Reilly, Philip; Davis, Ian C et al. (2002) Killing of Klebsiella pneumoniae by human alveolar macrophages. Am J Physiol Lung Cell Mol Physiol 282:L944-56 |
| Hickman-Davis, Judy M (2002) Role of innate immunity in respiratory mycoplasma infection. Front Biosci 7:d1347-55 |
| O'Reilly, Philip; Hickman-Davis, Judy M; McArdle, Philip et al. (2002) The role of nitric oxide in lung innate immunity: modulation by surfactant protein-A. Mol Cell Biochem 234-235:39-48 |
| Hickman-Davis, J M; Lindsey, J R; Matalon, S (2001) Cyclophosphamide decreases nitrotyrosine formation and inhibits nitric oxide production by alveolar macrophages in mycoplasmosis. Infect Immun 69:6401-10 |
| Hickman-Davis, J M (2001) Implications of mouse genotype for phenotype. News Physiol Sci 16:19-22 |
| Hickman-Davis, J; Matalon, S (1999) Surfactant protein B deficiency worsens hyperoxic injury to the alveolar epithelium. Am J Respir Cell Mol Biol 21:449-50 |
