A photo of Ty Troutman.

Ty D. Troutman, PhD

  • Assistant Professor, UC Department of Pediatrics



My research broadly focuses on innate immunity and the contribution of inflammation to acute and chronic disease. My specific research goals are to define the molecular mechanisms controlling the functions of macrophages and myeloid cells during illness. In my lab, we often apply diverse genomics technologies to purified tissue cells. With this strategy, we aim to decode transcriptional changes observed during disease by identifying the responsible transcription factors, upstream signaling pathways and sender cell populations.

I have used this strategy successfully to 1) identify a hierarchical framework controlling niche specification of macrophages, 2) discover transcriptional mechanisms controlling functional diversification of macrophages during nonalcoholic steatohepatitis, and 3) predict cis and trans-acting factors promoting response differences from genetically diverse individuals. This framework requires the tool kit of a cellular immunologist, a molecular biologist and a computational biologist.

I've been a researcher for over 17 years and started working at Cincinnati Children’s in 2021. Throughout my career, I have been fortunate to receive support from many scientific mentors. At the University of Texas (UT) at San Antonio, I was trained by Drs. Bernard Arulanandam and M. Neal Guenztel, while studying the immunological regulation of Vibrio cholerae pathogenesis. This experience established my desire for a career in science. I performed doctoral research under Dr. Chandrashekhar Pasare at UT Southwestern, defining new signaling mechanisms through the Toll-like receptor/interleukin one receptor (TLR/IL1R) superfamily. Finally, I trained with Dr. Christopher K. Glass at the University of California San Diego on gene regulation of macrophages during development and disease. These experiences have honed my value of scientific rigor and research mentorship, which I now use in my lab at Cincinnati Children’s.



Niche-Specific Reprogramming of Epigenetic Landscapes Drives Myeloid Cell Diversity in Nonalcoholic Steatohepatitis. Seidman, JS; Troutman, TD; Sakai, M; Gola, A; Spann, NJ; Bennett, H; Bruni, CM; Ouyang, Z; Li, RZ; Sun, X; et al. Immunity. 2020; 52:1057-1074.e7.


Liver-Derived Signals Sequentially Reprogram Myeloid Enhancers to Initiate and Maintain Kupffer Cell Identity. Sakai, M; Troutman, TD; Seidman, JS; Ouyang, Z; Spann, NJ; Abe, Y; Ego, KM; Bruni, CM; Deng, Z; Schlachetzki, JC M; et al. Immunity. 2019; 51:655-670.e8.


BCAP links IL-1R to the PI3K-mTOR pathway and regulates pathogenic Th17 cell differentiation. Deason, K; Troutman, TD; Jain, A; Challa, DK; Mandraju, R; Brewer, T; Ward, ES; Pasare, C. Journal of Experimental Medicine. 2018; 215:2413-2428.


Tissue damage drives co-localization of NF-κB, Smad3, and Nrf2 to direct Rev-erb sensitive wound repair in mouse macrophages. Eichenfield, DZ; Troutman, TD; Link, VM; Lam, MT; Cho, H; Gosselin, D; Spann, NJ; Lesch, HP; Tao, J; Muto, J; et al. eLife. 2016; 5.


Role for B-cell adapter for PI3K (BCAP) as a signaling adapter linking Toll-like receptors (TLRs) to serine/threonine kinases PI3K/Akt. Troutman, TD; Hu, W; Fulenchek, S; Yamazaki, T; Kurosaki, T; Bazan, JF; Pasare, C. Proceedings of the National Academy of Sciences of the United States of America. 2012; 109:273-278.

Systematic analysis of transcriptional and epigenetic effects of genetic variation in Kupffer cells enables discrimination of cell intrinsic and environment-dependent mechanisms. Bennett, H; Troutman, T; Zhou, E; Spann, N; Link, V; Seidman, J; Nickl, C; Abe, Y; Sakai, M; Pasillas, M; et al. 2022.

Exploiting dynamic enhancer landscapes to decode macrophage and microglia phenotypes in health and disease. Troutman, TD; Kofman, E; Glass, CK. Molecular Cell. 2021; 81:3888-3903.

Heterogeneity of HSCs in a Mouse Model of NASH. Rosenthal, SB; Liu, X; Ganguly, S; Dhar, D; Pasillas, MP; Ricciardelli, E; Li, RZ; Troutman, TD; Kisseleva, T; Glass, CK; et al. Hepatology. 2021; 74:667-685.

An optimized protocol for rapid, sensitive and robust on-bead ChIP-seq from primary cells. Texari, L; Spann, NJ; Troutman, TD; Sakai, M; Seidman, JS; Heinz, S. STAR Protocols. 2021; 2.

Purification of mouse hepatic non-parenchymal cells or nuclei for use in ChIP-seq and other next-generation sequencing approaches. Troutman, TD; Bennett, H; Sakai, M; Seidman, JS; Heinz, S; Glass, CK. STAR Protocols. 2021; 2.