Chad Steele, PhD
|
|
Professor of Medicine Division of Pulmonary, Allergy & Critical Care Medicine |
|
|
Contact Information |
||
|
Campus Address: |
THT 422 |
|
|
Academic Office location: |
THT 437-A |
|
|
Office Phone: |
(205) 996-9598 |
|
|
Office Fax (Academic): |
(205) 934-1721 |
|
|
Email Address: |
This email address is being protected from spambots. You need JavaScript enabled to view it. |
|
|
Lab Assistant: |
||
|
Brief Bio Dr. Claude H. (Chad) Steele III was born in Pensacola, Florida in 1972 and his family moved to northeast Louisiana the following year. Dr. Steele attended the University of Louisiana at Monroe (formerly Northeast Louisiana University), receiving a Bachelor's degree in Chemistry in 1995. After an 18 month stint as an industrial chemist, Dr. Steele entered graduate school in the Department of Microbiology at Louisiana State University Health Sciences Center-New Orleans, earning a Masters degree in December 1998, followed by a Doctorate in December 2000, both under the mentorship of Dr. Paul Fidel. Dr. Steele remained at LSUHSC for his post-doctoral fellowship, conducting lung host defense research in the laboratories of Dr. Jay Kolls and Dr. Judd Shellito. In July 2003, Dr. Steele was recruited as faculty to the Department of Pediatrics at the University of Pittsburgh, where he remained until June 2007. In July 2007, Dr. Steele was recruited to join the faculty at the University of Alabama at Birmingham, in the Division of Pulmonary, Allergy & Critical Care Medicine, where is currently a tenured Associate Professor of Medicine, Microbiology and Pathology. |
||
|
Research Interests Research in Dr. Steele's Laboratory of Lung Immunology and Host Defense is focused on understanding myeloid cell-mediated innate immune responses against opportunistic fungal pathogens that cause life-threatening lung infections in immunocompromised individuals with such diseases as HIV, COPD and leukemia. Dr. Steele's research on the fungal pathogen Pneumocystis carinii has uncovered a novel Src tyrosine kinase signaling pathway that regulates the magnitude of the lung inflammatory response as well as change the pattern of alveolar macrophage activation. This pattern of macrophage activation, termed M2a, is associated with more efficient elimination of P. carinii from the lungs, yet has not been described in P. carinii host defense. Dr. Steele's research team is currently characterizing multiple M2a-associated innate host defense molecules in an effort to understand what influences alveolar macrophage effector responses against P. carinii. The overarching goal of this work is to uncover new innate immune pathways that can be therapeutically augmented in the setting of immunosuppression and immunodeficiency for the treatment of P. carinii pneumonia. In a second project, Dr. Steele's research team has discovered an essential role for a myeloid-associated fungal recognition receptor, Dectin-1, in lung innate immune responses to the fungal pathogen Aspergillus fumigatus. Dectin-1, which recognizes beta-glucan carbohydrates found in the cell wall of all medically-important fungi, controls the production of multiple inflammatory cytokines, including IL-17. Dr. Steele's lab has recently reported a role for IL-17 in A. fumigatus lung defense and has recently been awarded a 2-year ARRA R01 and a new, 4-year R01 focusing on the lung cell source of IL-17, which pathways drive the development of this cell population and the downstream IL-17-associated mechanisms that promote elimination of A. fumigatus from the lungs. |
||
|
Research Statement I was first exposed to the devastating morbidity and mortality caused by opportunistic fungal pathogens, particularly in the immunocompromised and immunosuppressed individual, in my graduate work. My early work was the first to describe the anti-fungal properties of mucosal epithelial cells and elucidated potential epithelial-associated mechanisms of why mucosal fungal infections with Candida albicans occurred during hormonal changes and in the setting of HIV/AIDS. In my post-doctoral work, I continued to investigate Pneumocystis carinii, an atypical fungal pathogen that initiates infection in the lungs. With recent advances and more aggressive usage of therapies targeting suppression of the immune system, infections with opportunistic fungal pathogens, such as Pneumocystis carinii and Aspergillus fumigatus, are now more common than ever before. Here, I discovered that the beta-glucan receptor Dectin-1 was the predominant pattern recognition receptor mediating the lung macrophage response to P. carinii, the leading cause of pneumonia in HIV/AIDS. In my faculty work, I have further extended the role of Dectin-1 to lung defense against A. fumigatus, the leading cause of mortality in patients receiving solid organ or hematopoietic cell transplants. Work-in-progress is now focusing on how innate immune responses to fungal pathogens are regulated in order to develop a better understanding of how these responses can be amplified to treat infections in susceptible individuals. My lab is dedicated to understanding host defense against fungal pathogens, a class of microorganisms that rarely receive much attention, but cause some of the most lethal infections known to afflict humans. |
||
|
Key Publications: Werner, J.L., M.A. Gessner, L.M. Lilly, M.P. Nelson, A.E. Metz, D. Horn, C.W. Dunaway, J. Deshane D.D. Chaplin, G.D. Brown, C.T. Weaver and C. Steele. Neutrophils produce IL-17A in a Dectin-1 and IL-23 dependent manner during invasive fungal infection. Infection and Immunity 79:3966-3977 (2011). PMID:21807912 **Spotlight Article – Articles of Significant Interest Selected from This Issue by the Editors, October 2011 Issue** Gessner, M.A., J.L. Werner, L.M. Lilly, M.P. Nelson, A.E. Metz, C.W. Dunaway, Y.R. Chan, W. Ouyang, G.D. Brown, C.T. Weaver and C. Steele. Dectin-1 dependent IL-22 contributes to early innate lung defense against Aspergillus fumigatus. Infection and Immunity 80:410-417 (2012). PMID: 22038916. **Spotlight Article – Articles of Significant Interest Selected from This Issue by the Editors, January 2012 Issue** Nelson, M.P., B.S. Christmann, A. Burg, C. Dunaway, A. Morris and C. Steele. Experimental Pneumocystis lung infection promotes M2a alveolar macrophage-derived MMP12 production. American Journal of Physiology – Lung Cellular and Molecular Physiology 303:L469-75 (2012). PMID:22773692 Lilly, L.M., M.A. Gessner, C.W. Dunaway, A.E. Metz, L.M. Schwiebert, C.T. Weaver, G.D. Brown and C. Steele. The beta-glucan receptor Dectin-1 promotes immunopathology during fungal allergy via IL-22. Journal of Immunology 189:3653-60 (2012). PMID:22933634 Steele, C. and F.L. Wormley. Immunology of Fungal Infections: Lessons from Animal Models. Current Opinion in Microbiology 15:413-9 (2012). PMID:22763286 |
||
