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| Jonathon P. Audia, Ph.D., professor of microbiology and immunology, is investigating the molecular pathogenesis of pneumonia, inflammation and sepsis. |
He and other University of South Alabama collaborators will use the funds to further investigate the molecular pathogenesis of pneumonia, inflammation and sepsis using his established Pseudomonas aeruginosa lung infection models.
Pioneering, interdisciplinary research efforts spearheaded through the USA College of Medicine Center for Lung Biology have produced evidence to suggest that Gram-negative and Gram-positive bacterial pneumonia triggers production of cytotoxic amyloids in the lung as a pathological mechanism that underlies organ failure and decreased mental function.
While amyloids are well-known causes of Alzheimer’s disease and related dementias, the links between pneumonia, amyloids and neurocognitive dysfunction is an emerging field of interest, Audia said.
As part of an ongoing National Institutes of Health funded study on the role of inflammasomes in protecting the lung during pneumonia and sepsis, Audia’s research team made the serendipitous discovery that caspase-1 is able to detoxify amyloids, negating their negative effects. Caspase-1 is a component of inflammasomes that promotes harmful inflammation in the body.
“This new avenue of research in my lab is due in large part to the efforts of Nicole Housley who developed the key biochemical and cell biology assays that laid critical ground work,” Audia said.
The proposed studies represent a new collaboration between Audia’s research group and the laboratory of David Weber, Ph.D., professor of physiology and cell biology.
Audia said the new collaboration will allow an extension of the biological relevance of the study by investigating the vascular pathology induced by the P. aeruginosa infection model.
