Jack Krieger, Ph.D.

Jack Krieger received a B.S. in engineering physics from the University of Illinois at Urbana-Champaign in 2012 and joined Dr. Botchwey’s lab at Georgia Tech later that fall. His research interest is manipulating inflammation to augment healing of injured tissues. To achieve this end, Jack is involved in collaborative work developing hydrogel materials that release immunomodulatory molecules at sites of injury. Jack’s recent studies demonstrate that pro-regenerative inflammation and microvascularization are achieved by hydrogel-mediated delivery of immunomodulatory proteins and synthetic sphingolipid analogs.

In ongoing work, Jack is focused on rotator cuff tears, specifically how post-injury inflammation affects rotator cuff muscle health and whether immunomodulatory strategies can improve muscle function.

In his spare time, Jack can be found outside or watching live music.

Caitlin Sok

Caitlin Powell Sok completed her undergraduate degree in biomedical engineering at Case Western Reserve University in Cleveland. She is in the MD/PhD program at Emory University and joined Dr. Botchwey’s lab in 2013. Caitlin’s work focuses on developing materials that tune the inflammatory response after injury to promote tissue healing and repair. In recently published work, she demonstrated that local delivery of specialized proresolving lipid mediators modulate immune cell recruitment and enhance post-injury vascular remodeling. In ongoing collaborative work, Caitlin is interested in creating a combined-delivery hydrogel system that is able to promote acceptance of transplanted tissue.

Molly Ogle, PhD

Jada Selma

Jada Selma completed her undergraduate degree in biomedical engineering at Mississippi State University in Starkville, MS. She joined Dr. Botchwey’s lab in 2012. Jada’s work focuses on elucidating the underlying cellular and molecular mechanisms behind pathological bone remodeling in sickle cell disease (SCD).  Previous transgenic sickle mouse model studies have shown that increased osteoclast activity and reduced mesenchymal stem cell (MSC) differentiation into osteoblasts contributes broadly to sickle bone disease (SBD). However, Jada’s project aims to link SBD to the finding that sphingolipid metabolism is dysregulated in SCD.  Sphingosine 1-phosphate (S1P), a type of sphingolipid that is upregulated in SCD, directs a wide array of cellular processes including, migration, cell-cell adhesion, survival, and proliferation. S1P has also been found to direct MSCs towards an osteogenic lineage and modulates their migration. Moreover, Jada is also investigating the role of cell-derived microparticle  internalization by osteoclastic precursors in contributing to pathologic bone resorption in SCD due to increased inflammation and proteolytic activity.   In ongoing collaborative work, Jada is interested in applying these concepts to determine potential therapeutic targets for SBD as well as to improve MSC therapy for other bone disorders

Claire Olingy, Ph.D.

METABOLOMICS AND PATHOBIOLOGY

We have devoted significant attention in recent years to the role of sphingolipid metabolism in sickle red blood cells. We have recently identified a novel mechanism of feed-forward inflammatory signaling in SCD whereby sickled RBC membrane strain increases the activity of sphingomyelinase (SMase), which contributes to membrane lipid composition and budding of cellular vesicles. This dysregulation of sphingolipid metabolism leads to the aberrant production and release of cell-derived microparticles (SS MVs). MVs have been described as transcellular delivery vehicles that can transfer receptors, adhesion molecules, kinases, and lipids between cells. We are also investigating a potential pathogenic role of SS MVs in bone and joint disorders including osteonecrosis of the femoral head (ONFH). Read More

SMART BIOMATERIALS

An additional interest is the development of “immunologically smart” biomaterials that can tune the regenerative potential of subpopulations of leukocytes to the needs defined by the injury microenvironment. Our goal is to harness the phenotypic complexity and the division of labor among innate immune cell subsets to amplify endogenous mechanisms of tissue repair. In one recent example, we have shown that diverting circulating non-classical monocytes to injury sites using extracellular matrix (ECM)-derived hydrogels promotes healing and inflammation resolution in musculoskeletal injuries. Read More

ENDOGENOUS TISSUE ENGINEERING

Our interest is to understand the microenvironmental factors that govern healing outcomes in musculoskeletal tissues and skin in order to harness endogenous mechanisms of repair. Efficient wound healing requires the angiogenic and fibrogenic activity of macrophages, which are derived at least in part from circulating monocytes that undergo differentiation post-extravasation. We focus specifically on unlocking the therapeutic potential of pro-regenerative monocyte subsets and their progeny. Learn More

 

Dr. Botchwey on Monocytes

Therapeutic Angiogenesis and Bone Regeneration with Natural and Synthetic Small Molecules