A photo of Senad Divanovic.

Member, Division of Immunobiology

Assistant Professor, UC Department of Pediatrics

513-636-0286

Biography & Affiliation

Biography

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:

  • The immune pathways underlying obesity development and adipocyte-immune like behavior
  • The immune pathways underling increased infectious susceptibility in obesity
  • Immunopathogenesis of NAFLD
  • Obesity-dependent vertical transmission of adverse offspring health outcomes
  • Immunopathogenesis of preterm birth
  • The role of thermoneutral housing on immune responses and disease pathogenesis

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:

  • 2012 Trustee Award, Cincinnati Children’s
  • 2018 Milstein Award, International Cytokine & Interferon Society (ICIS)
  • 2018 Top 7 Breakthrough Discoveries, Cincinnati Children’s
  • 2020 Cincinnati Children’s Research Foundation (CCRF) Endowed Scholar
  • 2018 Innovative Basic Science Award, American Diabetes Association (ADA)
  • 2015 Preterm Birth Initiative Award, Burroughs Wellcome Fund

Clinical Interests

Innate immune responses; obesity; NAFLD; preterm birth; echocardiography; fetal cardiology; Cardiology Consult Service; General Cardiology Outpatient Clinic

Academic Affiliation

Assistant Professor, UC Department of Pediatrics

Research Divisions

Immunobiology, Inflammation and Tolerance



Blog Posts

How a Fat Cell’s Immune Response Makes Obesity Worse

Diabetes and Obesity

How a Fat Cell’s Immune Response Makes Obesity Worse

Senad Divanovic, PhD6/2/2020

‘Thermoneutral’ Mouse Model Opens Doors for Obesity Research

Tools for Science

‘Thermoneutral’ Mouse Model Opens Doors for Obesity Research

Senad Divanovic, PhD7/3/2019

Education

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

Publications

Type I interferon sensing unlocks dormant adipocyte inflammatory potential. Chan, CC; Damen, MS M A; Moreno-Fernandez, ME; Stankiewicz, TE; Cappelletti, M; Alarcon, PC; Oates, JR; Doll, JR; Mukherjee, R; Chen, X; et al. Nature Communications. 2020; 11.

Type I interferon sensing unlocks dormant adipocyte inflammatory potential. Chan, CC; Damen, MS M A; Moreno-Fernandez, ME; Stankiewicz, TE; Cappelletti, M; Alarcon, PC; Oates, JR; Doll, JR; Mukherjee, R; Chen, X; et al. Nature Communications. 2020; 11.

Maternal regulation of inflammatory cues is required for induction of preterm birth. Cappelletti, M; Doll, JR; Stankiewicz, TE; Lawson, MJ; Sauer, V; Wen, B; Kalinichenko, VV; Sun, X; Tilburgs, T; Divanovic, S. JCI insight. 2020; 5.

Not Chopped Liver—A Careful, Fate-Mapping Study of Macrophages in NASH. Moreno-Fernandez, ME; Miraldi, ER; Divanovic, S. Cell Metabolism. 2020; 32:328-330.

Fructose and hepatic insulin resistance. Softic, S; Stanhope, KL; Boucher, J; Divanovic, S; Lanaspa, MA; Johnson, RJ; Kahn, CR. Critical Reviews in Clinical Laboratory Sciences (Informa). 2020; 57:308-322.

IL-10–producing Tfh cells accumulate with age and link inflammation with age-related immune suppression. Almanan, M; Raynor, J; Ogunsulire, I; Malyshkina, A; Mukherjee, S; Hummel, SA; Ingram, JT; Saini, A; Xie, MM; Alenghat, T; et al. Science Advances. 2020; 6:eabb0806-eabb0806.

Type I interferon sensing unlocks dormant adipocyte inflammatory potential. Chan, CC; Damen, MS M A; Moreno-Fernandez, ME; Stankiewicz, TE; Cappelletti, M; Alarcon, PC; Oates, JR; Doll, JR; Mukherjee, R; Chen, X; et al. Nature Communications. 2020; 11.

Macrophage Function in the Pathogenesis of Non-alcoholic Fatty Liver Disease: The Mac Attack. Oates, JR; McKell, MC; Moreno-Fernandez, ME; Damen, MS M A; Deepe, GS; Qualls, JE; Divanovic, S. Frontiers in Immunology. 2019; 10.

GWAS and enrichment analyses of non-alcoholic fatty liver disease identify new trait-associated genes and pathways across eMERGE Network. Namjou, B; Lingren, T; Huang, Y; Parameswaran, S; Cobb, BL; Stanaway, IB; Connolly, JJ; Mentch, FD; Benoit, B; Niu, X; et al. BMC Medicine. 2019; 17.

Short-term high-fat diet feeding protects from the development of experimental allergic asthma in mice. Schroeder, T; Wiese, AV; Ender, F; Quell, KM; Vollbrandt, T; Duhn, J; Suenderhauf, A; Kuenstner, A; Moreno-Fernandez, ME; Derer, S; et al. Clinical and Experimental Allergy. 2019; 49:1245-1257.