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Background

When I started graduate school at the University of California, Riverside (UCR), I became fascinated by the signaling networks regulating cell behavior.  After I joined the Martins-Green lab at UCR, I worked on multiple lines of research, focusing on the cell signaling that initiates inflammation and the signaling that causes inflammation to end.  After completing my PhD and a short postdoc in the same lab, I started teaching at the college level, beginning with a summer cell biology course at UCR, and then teaching at two community colleges, Chaffey College and Citrus College, as well as a liberal arts college, Pomona College.  These teaching experiences made me passionate about teaching and conducting research with undergraduate students, and when I arrived at DePauw University in 2015, I began several research projects involving undergraduates, explained in further detail below.  Apart from my academic interests in inflammation regulation and cell signaling, I enjoy playing board games, watching Doctor Who, and cooking (and eating!) spicy foods.

Lines of Research

The immune system is responsible for identifying and eliminating foreign organisms, like bacteria or fungi.  The first immune cells that are recruited from the blood in response to a foreign invader are the neutrophils, which, after they arrive in the infected/contaminated tissue, kill these microbes by “eating” them (phagocytosis), producing toxic molecules called reactive oxygen species (ROS) that damage them, or ensnare them in neutrophil extracellular traps (NETs) that trap them in a toxic environment.  While these anti-microbial strategies effectively destroy microbes, ROS and NETs also damage host cells (directly or indirectly), so these neutrophil functions must be limited to minimize host tissue damage.  In my lab, we are investigating multiple ways in which signaling proteins (TNFSF14), medications (anti-depressants), and food-derived nutraceutical molecules affect neutrophil cell functions.  Specifically, our work involves:

  • INTEREST A (ONGOING) - The regulation of neutrophil extracellular trap (NET) formation by the cytokine TNFSF14/LIGHT

  • INTEREST B (ONGOING) - The effect of anti-depressant drugs on neutrophil functions and inflammation (ongoing)

  • INTEREST C - The impact of nutraceuticals on neutrophil functions and inflammation


Regulation of neutrophil extracellular trap (NET) formation by the cytokine TNFSF14

In my lab, we have found that the signaling molecule TNFSF14 can decrease NET formation in neutrophil-like cells, but we do not yet understand how TNFSF14 exerts this effect.  We are currently investigating the role of a cellular “self-eating” process called autophagy on the inhibition of NET formation by TNFSF14.  Because NETs increase inflammation and host tissue damage, the generation of NETs may be responsible, at least in part, for the painful and damaging symptoms associated with inflammatory diseases.  If so, inhibition of NET formation by molecules like TNFSF14 could reduce the symptoms such diseases, increasing the quality of life for people with these diseases.

STUDENT COLLABORATION

    • Liz Aguilar, Maddie Smith, Michelle Wiebe, Nathalia Melo, and Bob Berwanger, TNFSF14 and ROS production

    • Breanna Kloczkowski, TNFSF14 and neutrophil apoptosis

 

The effect of anti-depressant drugs on neutrophil functions and inflammation

Certain anti-depressant drugs, the selective serotonin reuptake inhibitors (SSRIs), have anti-inflammatory properties that can be useful in treating excessive inflammation.  The mechanisms used by SSRIs to limit inflammation include decreasing neutrophil recruitment to damaged tissues, decreasing neutrophil ROS production, reducing the production of pro-inflammatory proteins called cytokines, and increasing neutrophil cell death, although the mode of neutrophil cell death remains unclear.  Our lab began investigating the ability of fluoxetine (Prozac™), an SSRI, to induce one specific mode of neutrophil cell death, apoptosis.  We found that fluoxetine does induce apoptosis in neutrophil-like cells.  The ability of SSRIs to simultaneously increase neutrophil apoptosis and decrease ROS production suggests that SSRIs may decrease NET production, which frequently requires ROS production and is incompatible with apoptosis.  The next step of this study involves determining whether SSRIs reduce NET production.  If correct, SSRIs may reduce inflammation, at least in part, through their ability to decrease NET production.

STUDENT COLLABORATION

    • John Daseke, fluoxetine and neutrophil apoptosis

 

The impact of nutraceuticals on neutrophil functions and inflammation

Specific molecules present in various types of foods, termed “nutraceuticals,” have anti-inflammatory properties; however, the mechanisms through which many nutraceuticals reduce inflammation are incompletely understood.  One area of interest in my lab involves characterizing the mechanisms used by specific nutraceuticals to reduce inflammation, which allows individual students to identify their own nutraceutical of interest and then design and conduct experiments to determine whether that nutraceutical decreases neutrophil behaviors associated with inflammation, such as ROS or NET production, and/or increases neutrophil behaviors associated with the resolution of inflammation, such as neutrophil apoptosis.  These studies have important implications in our understanding of the connections between the foods that we eat and our inflammatory processes.

STUDENT COLLABORATION

    • Nina Moore, ginger-derived compounds and neutrophil ROS and NET production Student Research

 

 

 

 

 

 

 

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