The lab's early work focused on understanding fundamental cellular processes using microbial systems and bacterial virulence factors as molecular tools. Research investigated bacterial regulatory mechanisms as well as how Pseudomonas aeruginosa toxins alter mammalian cell biology.

A major focus was the use of the P. aeruginosa Type III secretion effector ExoT to uncover mechanisms controlling cytokinesis, apoptosis, focal adhesion signaling, and cell survival. Studies demonstrated that ExoT can interfere with multiple stages of mammalian cytokinesis and induce apoptosis, providing important insights into fundamental host-cell processes.

Key themes:

Cytokinesis • Apoptosis • Cell signaling • Bacterial toxins • Host-cell biology

The research program expanded from understanding individual cellular mechanisms to investigating how bacterial virulence strategies influence infection, tissue injury, and host defense.

The lab investigated how P. aeruginosa Type III secretion system effectors manipulate host cells, including mechanisms involving ExoT, apoptosis, cytoskeletal signaling, and cellular survival. This work also established important connections between bacterial virulence and impaired wound healing. For example, the lab demonstrated that P. aeruginosa uses its Type III secretion system to inhibit diabetic wound healing.

During this period, the laboratory also began investigating surgical-site infection and immune-based approaches to infection control, laying the foundation for later therapeutic studies.

Key themes:
Pseudomonas pathogenesis • Virulence mechanisms • Innate immunity • Infection • Wound healing

Diabetic Wounds, Metabolic Dysfunction & Precision Immunology

The lab's current research focuses on understanding why diabetic wounds fail to control infection and heal effectively. Building on earlier discoveries of impaired neutrophil and macrophage responses, the laboratory is now investigating how diabetes-associated metabolic dysfunction alters cellular function and the wound-healing environment.

A major ongoing direction is to determine how metabolic disturbances associated with diabetes affect the coordinated responses required for successful wound repair. The lab is investigating how altered cellular metabolism may influence immune-cell function, inflammatory signaling, tissue repair, and host–microbe interactions, ultimately contributing to persistent inflammation, increased susceptibility to infection, and delayed wound healing.

To resolve these complex cellular changes, the lab is incorporating single-cell transcriptomic analysis to characterize cell-type-specific molecular programs within diabetic wounds. This approach enables the identification of distinct cellular populations and dysfunctional gene-expression programs that may be masked in bulk tissue analysis. By integrating single-cell profiles with experimental wound-healing and infection models, the research aims to identify cellular and molecular pathways that drive impaired healing in diabetes.

These mechanistic studies complement the laboratory's therapeutic research, including CCL3-based immunomodulatory approaches, with the broader goal of identifying ways to restore dysfunctional host responses and improve infection control and tissue repair.

Key themes

Metabolic Dysfunction • Single-Cell Biology • Immune-Cell Dysfunction • Diabetic Wounds • Host–Microbe Interactions • Immunomodulatory Therapies • Wound Healing