Sean P. Colgan

Control of creatine metabolism by HIF is an endogenous mechanism of barrier regulation in colitis.

IFN-γ-mediated induction of an apical IL-10 receptor on polarized intestinal epithelia.

Neutrophils and inflammatory metabolism in antimicrobial functions of the mucosa.

HIF-dependent regulation of claudin-1 is central to intestinal epithelial tight junction integrity.

Actions of adenosine on cullin neddylation: implications for inflammatory responses.

Creatine kinase in ischemic and inflammatory disorders.

Tryptophan metabolite activation of the aryl hydrocarbon receptor regulates IL-10 receptor expression on intestinal epithelia.

Intestinal Epithelial Ecto-5'-Nucleotidase (CD73) Regulates Intestinal Colonization and Infection by Nontyphoidal Salmonella.

Neutrophils as sources of dinucleotide polyphosphates and metabolism by epithelial ENPP1 to influence barrier function via adenosine signaling.

Subversion of Systemic Glucose Metabolism as a Mechanism to Support the Growth of Leukemia Cells.

Cholestatic liver disease results increased production of reactive aldehydes and an atypical periportal hepatic antioxidant response.

Intense Light-Mediated Circadian Cardioprotection via Transcriptional Reprogramming of the Endothelium.

Hypoxia-Inducible Factor-2α Reprograms Liver Macrophages to Protect Against Acute Liver Injury Through the Production of Interleukin-6.

Adaptation to inflammatory acidity through neutrophil-derived adenosine regulation of SLC26A3.

Hypoxia and Innate Immunity: Keeping Up with the HIFsters.

Microbiota-derived butyrate dynamically regulates intestinal homeostasis through regulation of actin-associated protein synaptopodin.

Microbiota-Sourced Purines Support Wound Healing and Mucous Barrier Function.

Bile acids modulate colonic MAdCAM-1 expression in a murine model of combined cholestasis and colitis.

Eosinophils attenuate hepatic ischemia-reperfusion injury in mice through ST2-dependent IL-13 production.

Microbial-derived indoles inhibit neutrophil myeloperoxidase to diminish bystander tissue damage.

Mucosal acidosis elicits a unique molecular signature in epithelia and intestinal tissue mediated by GPR31-induced CREB phosphorylation.