My research aims to identify critical knowledge gaps that link immune responses with inflammatory, infectious and metabolic diseases. I gained expertise through the pursuit of studies arising from the reductive analysis of both innate and adaptive immune responses (e.g., TLR, BAFF, Type I IFN and IL-17 signaling) in animal models. These experiences have positioned me well to lead projects aimed at defining the mechanisms underlying immunopathogenesis of various diseases.
Research areas that interest me include immunology, immunometabolism, obesity, non-alcoholic fatty liver disease (NAFLD) and preterm birth. I began my independent research career work at Cincinnati Children's in 2010. My research has been supported by the National Institutes of Health (NIH) since 2013.
The overall goal of my research program is to define the fundamental processes, mechanisms and immune pathways underlying disease pathogenesis. My ultimate objective is translational exploitation of such insights for reducing or eliminating the burden of inflammation-associated diseases.
Specifically, the focus of my laboratory is to exploit:
Further, our experimental models are supported by established and ever-developing platforms of primary human samples from individuals clinically stratified into respective disease categories.
Some of my most notable discoveries include identifying RP105 as a negative regulator of TLR4 signaling, demonstrating how IL-17 axis functions in the regulation of NAFLD progression and employing thermoneutrality as an improved, more “human-like” approach, to study inflammatory and metabolic diseases.
It is my honor to have received several awards, including:
BA: DePauw University, Greencastle, IN, 1998.
MS: Oklahoma State University, Stillwater, OK, 2000.
PhD: University of Cincinnati, Cincinnati, OH, 2005.
Post Doc: Cincinnati Children’s Hospital Medical Center, 2010
Innate immune responses; obesity; NAFLD; preterm birth; echocardiography; fetal cardiology; Cardiology Consult Service; General Cardiology Outpatient Clinic
Immunobiology, Inflammation and Tolerance
Thermoneutral housing shapes hepatic inflammation and damage in mouse models of non-alcoholic fatty liver disease. Frontiers in Immunology. 2023; 14.
Fructose Induced KHK-C Increases ER Stress and Modulates Hepatic Transcriptome to Drive Liver Disease in Diet-Induced and Genetic Models of NAFLD. 2023.
In vivo generation of bone marrow from embryonic stem cells in interspecies chimeras. eLife. 2022; 11.
Greasing the inflammatory pathogenesis of viral pneumonias in diabetes. Obesity Reviews. 2022; 23.
Microbial metabolite butyrate promotes induction of IL-10+IgM+ plasma cells. PLoS ONE. 2022; 17.
A protocol for isolation of primary human immune cells from the liver and mesenteric white adipose tissue biopsies. STAR Protocols. 2021; 2.
A BAFF/APRIL axis regulates obesogenic diet-driven weight gain. Nature Communications. 2021; 12.
Adipocyte inflammation and pathogenesis of viral pneumonias: an overlooked contribution. Mucosal Immunology. 2021; 14:1224-1234.
Non-hematopoietic IL-4Rα expression contributes to fructose-driven obesity and metabolic sequelae. International Journal of Obesity. 2021; 45:2377-2387.
Implications of Inflammatory States on Dysfunctional Immune Responses in Aging and Obesity. 2021; 2.
Senad Divanovic, PhD5/18/2021
Senad Divanovic, PhD5/17/2021
Senad Divanovic, PhD6/2/2020
Senad Divanovic, PhD7/3/2019