Bethany Moore, PhD
The success of hematopoietic stem cell transplant (HSCT) therapy is severely limited by pulmonary complications, including Pseudomonas aeruginosa and Streptococcus pneumoniae. We demonstrated that mice which have fully reconstituted their hematopoietic compartment including alveolar macrophages (AMs) post-bone marrow transplantation (BMT) have impaired host defense against the Gram negative pathogen P. aeruginosa. Impaired innate immunity is related, in part, to increased production of prostaglandin E2 (PGE2) by AMs. Cyclooxygenase (COX)-2 is the rate-limiting enzyme for synthesis of PGE2 from arachidonic acid, and COX-2 expression is elevated in AMs post-BMT. Furthermore, we have also observed changes in scavenger receptor profiles which may be affecting macrophage function post-transplant. Alterations in miRNA expression also observed after transplant may explain the changes in scavenger receptor expression. Therefore, we hypothesized that epigenetic mechanisms and miRNA alterations may be responsible for the defect in BMT AMs.
Racquel Domingo-Gonzalez, Steven Huang, Yasmina Laouar, Bethany B. Moore. Hypomethylation of the Cox-2 promoter upregulate COX-2 and PGE2 levels post-bone marrow transplant. American Association of Immunologists Conference. Boston, MA, May 4-8 2012.
Racquel Domingo-Gonzalez, Steven Huang, Bethany Moore. Methylation patterns of Cox-2 promoter affect Cox-2 and PGE2 levels post-bone marrow transplant. Autumn Immunology Conference, Chicago, IL, November 20-23 2011.
John Wallace Diversity Award, 2011