Charles A. Parkos

Challenges in IBD Research: Update on Progress and Prioritization of the CCFA's Research Agenda.

Junctional adhesion molecule A promotes epithelial tight junction assembly to augment lung barrier function.

Annexin A1-containing extracellular vesicles and polymeric nanoparticles promote epithelial wound repair.

HNF4α regulates claudin-7 protein expression during intestinal epithelial differentiation.

Inflammation-induced desmoglein-2 ectodomain shedding compromises the mucosal barrier.

Cutting Edge: IL-36 Receptor Promotes Resolution of Intestinal Damage.

Targeting of Neutrophil Lewis X Blocks Transepithelial Migration and Increases Phagocytosis and Degranulation.

Neutrophil-Epithelial Interactions: A Double-Edged Sword.

Loss of Junctional Adhesion Molecule A Promotes Severe Steatohepatitis in Mice on a Diet High in Saturated Fat, Fructose, and Cholesterol.

Redox control of Cas phosphorylation requires Abl kinase in regulation of intestinal epithelial cell spreading and migration.

Inflammation and the Intestinal Barrier: Leukocyte-Epithelial Cell Interactions, Cell Junction Remodeling, and Mucosal Repair.

Deposition of microparticles by neutrophils onto inflamed epithelium: a new mechanism to disrupt epithelial intercellular adhesions and promote transepithelial migration.

Pathobiology of neutrophil-epithelial interactions.

Claudin-based barrier differentiation in the colonic epithelial crypt niche involves Hopx/Klf4 and Tcf7l2/Hnf4-α cascades.

IL-17A-mediated neutrophil recruitment limits expansion of segmented filamentous bacteria.

Defects in CD4+ T cell LFA-1 integrin-dependent adhesion and proliferation protect Cd47-/- mice from EAE.

Expression of Lewis-a glycans on polymorphonuclear leukocytes augments function by increasing transmigration.

Macrophage-derived IL-10 mediates mucosal repair by epithelial WISP-1 signaling.

Role of negative regulation of immune signaling pathways in neutrophil function.

Intracellular Desmoglein-2 cleavage sensitizes epithelial cells to apoptosis in response to pro-inflammatory cytokines.

Estrogen Receptor-Alpha (ESR1) Governs the Lower Female Reproductive Tract Vulnerability to .

Analysis of leukocyte transepithelial migration using an in vivo murine colonic loop model.

Role of JAM-A tyrosine phosphorylation in epithelial barrier dysfunction during intestinal inflammation.

Macrophage-dependent neutrophil recruitment is impaired under conditions of increased intestinal permeability in JAM-A-deficient mice.

Gab2 and Gab3 Redundantly Suppress Colitis by Modulating Macrophage and CD8 T-Cell Activation.

TNFα promotes mucosal wound repair through enhanced platelet activating factor receptor signaling in the epithelium.

Innate immune cell-epithelial crosstalk during wound repair.

Formyl peptide receptor 2 regulates monocyte recruitment to promote intestinal mucosal wound repair.

Epithelial CD47 is critical for mucosal repair in the murine intestine in vivo.

Regulation of neutrophil function by selective targeting of glycan epitopes expressed on the integrin CD11b/CD18.

Desmocollin-2 promotes intestinal mucosal repair by controlling integrin-dependent cell adhesion and migration.

Western diet-induced increase in colonic bile acids compromises epithelial barrier in nonalcoholic steatohepatitis.

Resolvin E1 is a pro-repair molecule that promotes intestinal epithelial wound healing.

Targeting epithelial expressed Sialyl Lewis glycans improves colonic mucosal wound healing and protects against colitis.

Blocking integrin αβ-mediated CD4 T cell recruitment to the intestine and liver protects mice from western diet-induced non-alcoholic steatohepatitis.

Neutrophil expressed CD47 regulates CD11b/CD18-dependent neutrophil transepithelial migration in the intestine in vivo.

Dysregulation of intestinal epithelial CFTR-dependent Cl ion transport and paracellular barrier function drives gastrointestinal symptoms of food-induced anaphylaxis in mice.

WD40 Repeat Protein 26 Negatively Regulates Formyl Peptide Receptor-1 Mediated Wound Healing in Intestinal Epithelial Cells.