Chad Steele
Contact
Medicine
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Other information
Other information:
Phone: (205) 996-9598
Ph.D. (Microbiology) 2000, Louisiana State University Health Sciences Center-New Orleans
STATUS: Currently has open positions for undergraduates.
STATUS: Currently has open positions for undergraduates.
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 andAspergillus 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.
To find out more about Dr. Steele's research please visit here