Inhibition of Mycobacterium tuberculosis Induced Bone Erosion by the Novel Compound ELP-004

Kendyl Berry*, Jamie McCall, and John Barnett
Department of Microbiology, Immunology, and Cell Biology

Presentation No.: 7

Assigned Category (Presentation Format): Biological & Health Sciences (Oral Presentations)

Student’s Major: Immunology and Medical Microbiology

Mycobacterium tuberculosis (MTB) induces a serious bacterial infection, tuberculosis (TB). Although TB primarily attacks the lungs, this bacteria can spread throughout the body, causing a form of arthritis resulting in soft-tissue swelling, joint effusion, and bone erosion, referred to as tuberculosis arthritis (TA). Bone erosion associated with TA is resultant of enhanced osteoclast activity by the MTB infection. In a healthy person, osteoclasts work in conjunction with osteoblasts to remove old bone as new bone is created, in arthritis, this balance is skewed. A novel compound, ELP-004, was shown to inhibit osteoclast induction in vitro and reduce disease severity in animal models of arthritis. We hypothesized that ELP-004 would also reduce the formation of MTB-induced multinucleated cells. To test whether ELP-004 prevented MTB-induced osteoclastogenesis, RAW 264.7 cells were treated using a non-infectious strain of MTB, H37RV, with and without ELP-004 and with RANKL as a positive control. Experimentation showed that while MTB treated cells do form multinucleated cells morphologically resembling osteoclasts, further investigation is necessary to classify and determine the function of TB-induced multinucleated cells.

Funding: NIH AR074812

Program/mechanism supporting research/creative efforts: the WVU IMMB Undergraduate Research Internship Program (Jennifer Franko)