Logo for University of Iowa Health Care This logo represents the University of Iowa Health Care

PhD candidate Allan Prichard successfully passes his PhD defense

Allan Prichard micro passes defense image with mentor Lee Ann Allen

On October 21, 2022. Allan Prichard successfully defended his thesis titled, "Effects of Helicobacter pylori Induced Neutrophil Subtype Differentiation on Chemotaxis and Phagosome Maturation”.  He is pictured with his mentor Lee-Ann Allen, PhD.  



Allen Scot Prichard was born in Lakeville, Minnesota, the third of four children to Lori Perkins and Scot Prichard. His family moved twice during childhood, with a short stint in Richmond, VA, before settling in Muskego, WI. In Muskego, he attended school from elementary to high school, during which time his love for Science began. This likely resulted from a childhood nightly routine in which Allan's father Scot would tell him something interesting in the scientific field before bed. While this was frequently related to computer science facts, it quickly evolved to cover various aspects of Science. 

This desire for knowledge and interest in biology led him to attend the University of Wisconsin-Madison, pursuing a degree in Microbiology. With his bachelor's degree, his love for microbiology and benchwork flourished. This resulted in two publications in Laura Hernandez's laboratory, which focused on lactation biology and endocrinology. During this time, he also served as the UW-Madison Microbiology Club president and outreach committee leader, in which he communicated science to children in the Madison area at Science Saturdays. Additionally, he attended a short summer internship at the University of Alabama at Birmingham, focusing on drug discovery in emerging viral infections. 

After graduation, Allan matriculated to the University of Iowa, where he began his dissertation in the laboratory of Dr. Lee-Ann Allen. During his schooling, the laboratory moved twice, to EMRB in 2018 and finally to the University of Missouri in 2020. His graduate work focused on determining the effects of neutrophil subtype differentiation on cell function during Helicobacter pylori infection. His studies resulted in a focus on cell migration and phagosome maturation during infection. Allan was fortunate enough to present his research at 13 conferences in graduate school as both an invited speaker and poster presenter resulting in several awards. Allan's research resulted in one first-author manuscript and one mid-author manuscript. Currently, Allan is interviewing for positions in industry where he intends to continue research in Microbiology and Immunology. 

Outside the lab, Allan enjoys getting lost in nature hiking with his golden retriever Fynn and mountain biking local trails. He also has a special appreciation for food, which resulted in multiple road trips to St. Louis. Additionally, he is what some would term a football fanatic attending multiple Wisconsin-Iowa football games during graduate school (Go Badgers!).


Helicobacter pylori is Gram-negative bacterial pathogen that colonizes the gastric mucosa of 50% of the global population. Once acquired this bacterium typically persists for the life of the individual and plays a causative role in the development of peptic ulcers and gastric cancer. While infection often remains asymptomatic it evokes histological gastritis characterized by a neutrophil-dominant inflammatory response. Remarkably, the neutrophil-dominant immune response fails to resolve infection instead resulting in the accumulation of heavily infected cells. Our lab discovered that H. pylori infection induces an N-1 like subtype differentiation that is characterized by a notable progressive nuclear hypersegmentation. While the field of neutrophil differentiation is currently advancing, the functionality of these subtypes is largely unknown.

My thesis work demonstrates that H. pylori infected neutrophils exhibit defective chemotaxis that precedes hypersegmentation. Our data reveal failed uropod retraction in a 2-D model, that was characterized by aberrant actin structures and mislocalized myosin machinery. This phenotype resembled myosin machinery inhibitors, however, analysis of myosin activation by immunoblotting revealed significantly increased myosin activation during infection. Interestingly, calcium signaling and integrin-mediated adhesion were unchanged suggesting a more complicated mechanism. Furthermore, H. pylori gastric epithelial virulence effectors were dispensable to defective chemotaxis we speculate that impaired migratory capacity may account for infection confinement to the gastric mucosa.

As migration is an essential function to PMN phagocytic capacity, and H. pylori displays intracellular persistence we examined phagocytosis and phagosome maturation during this infection. This revealed failed phagosome maturation through inhibited granule-phagosome fusion and favored global granule exocytosis. Infection was further characterized by CEACAM recruitment during ingestion, in addition to phagosome accumulation of autophagy protein LC3. Taken together the data in this thesis supports a model of impaired differentiated PMN function that results in failed bacterial clearance and gastric mucosa persistence despite a robust cellular response.


Thursday, October 27, 2022