Date of Award


Degree Type


Degree Name

Master of Science in Microbiology



First Advisor

Jay Sperry


A possible mechanism of pathogenicity of Bacteroides fragilis was determined while studying interaction of rabbit peritoneal polymorphonuclear neutrophils (PMN neutrophils) with Bacteroides products (outer membrane and culture supernatant of B. fragilis VPI 9032, VPI 2553 and B. vulgatus VPI 4245; culture supernatant of B. thetaiotaomicron VPI 5482; and LPS of B. fragilis VPI 9032). Neutrophils were elicited by injection of glycogen into the peritoneal cavity of rabbits and harvested four to seven hours later.

When rabbit peritoneal neutrophils were exposed to Bacteroides products, the neutrophils released N-acetyl-β-glucosaminidase, a lysosmal enzyme. Bacteroides products also induced directional locomotion (chemotaxis) of rabbit PMN neutrophils in Boyden chambers. The chemotactic response of rabbit neutrophils was dependent on the dosages of Bacteroides stimulant.

The enzyme release response was greatly enhanced when Bacteroides products were pre-incubated at 37°C for 30 minutes with equal volumes of fresh guinea pig complement. However, when Bacteroides outer membrane or sterile culture supernatants were pre-incubated with fresh guinea pig compliment, PMN neutrophil chemotaxis was retarded.

Lactate dehydrogenase (a cytoplasmic marker) was not released upon exposure of rabbit PMN neutrophils to Bacteroides products. This indicated that the response to Bacteroides products reflect an active extracellular secretion of PMN neutrophil lysosmal contents rather than a non-specific discharge of enzymes as a result of cell (PMN neutrophil) death.

These findings suggest an altered inflammatory response to neutrophils during the interaction of Bacteroides with the host defense mechanism.



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