As a member of the Chaaban laboratory, Dr. Eckert implemented a model of and neonatal necrotizing enterocolitis (NEC), and has focused in developing other experimental models through which to study diseases of NIH pre-doctoral training fellowship/scholarship intestinal inflammation. A recent focus has includes exploring acute kidney injury (AKI) in NEC. In addition, Dr. Eckert assists with multiple translation projects, clinical studies, and is a co-director for the biorepository.
Ph.D. - Medical College of Wisconsin Department of Physiology (Center for Human Molecular Genetics), Milwaukee, WI
Postdoctoral Fellowship - University of Oklahoma Health Sciences Center, Oklahoma City, OK
The Chaaban laboratory works to elucidate the mechanisms through which glycosaminoglycans (GAGs), biologically active components of breast milk, may be protective against intestinal inflammation generally, and neonatal necrotizing enterocolitis (NEC). Research in the Chaaban laboratory has focused on the many risk factors at play in predisposing infants to developing NEC, including extensive use of antibiotics, lack of breastfeeding, disrupted intestinal microbiome, and the developmentally immature interface between the immune system and the intestinal epithelium in the neonate. Both rodent models and in vitro systems are utilized to further investigate specific attributes of many of these risk factors in the hope that effective therapeutic strategies against NEC and associated diseases will surface.
Recent work has begun to explore AKI in NEC. Recent data from human and animal studies show that approximately 12% of preterm infants develop AKI, defined by a raise in serum creatinine from a previous low. In two independent studies, 50% of infants who developed NEC stage 2 or above developed kidney injury with more severe NEC identified as a risk factor for AKI. Interestingly, AKI was an independent risk factor for mortality, demonstrating that AKI in NEC patients is not a silent player but actually an active contributor to worse outcomes. We are working to determine the extent of acute renal injury will be observed in the Paneth cell ablation model of NEC. NEC leads to a systemic inflammatory response not only in the gut but also possibly in the kidney. We are exploring the kidney damage within our NEC model exploring histological injury, inflammation and disruption of tight junction proteins. In addition, we are also exploring pathways of inflammation and metabolism within the kidney in a NEC model.
Select Honors & Accomplishments:
2019 - Mentor Award Pediatrics Research Day
2017 - Mentor Award Pediatrics Research Day
2016 - Mentor Award Pediatrics Research Day
2015 - Mentor Award Pediatrics Research Day
2002-2006 - NIH pre-doctoral training fellowship/scholarship
2004 - NSF Research Experience for Undergraduates (REU)
- Chaaban H, Burge K, Eckert J, Keshari R, Silasi-Mansat R, Lupu C, Warner B, Escobedo M, Caplan M, Lupu F. Neutrophil extracellular trap inhibition increases inflammation, bacteremia, and mortality in murine necrotizing enterocolitis. J Cell Molec Med (Online Ahead of Print), 2020. PMID 32515131.
- Eckert J, Scott B, Lawrence SM, Ihnat M, Chaaban H. FLLL32, a curcumin analog, ameliorates intestinal injury in necrotizing enterocolitis. J Inflamm Res. 2017 Jun 14;10:75-81. PMID: 28652797
- Gunasekaran A, Eckert J, Burge K, Zheng W, Yu Z, Kessler S, de la Motte C, Chaaban H. Hyaluronan 35 kDa enhances epithelial barrier function and protects against the development of murine necrotizing enterocolitis. Ped Res 87(7), 177-1184, 2019. PMID 31499514. PMC7061074.