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<p>Outer membrane vesicles are an important constitutive product of all Gram-negative
bacteria. Bacteria have evolved many responses to alleviate all different types of
stress. The primary objective of this dissertation is to investigate the role of outer
membrane vesicles (OMVs) as a method by which Gram-negative bacteria can quickly act
to protect themselves against particular threats. Generally, we find that stressors
whose primary effect is on the outer membrane can be protected against by OMVs. Throughout
this study, a variety of different microbiological and biochemical methods are used
to answer key questions in the innate ability of OMVs to protect against particular
antimicrobials. Using Escherichia coli as well as Pseudomonas aeruginosa as model
organisms we tested the ability of purified vesicles from each species to protect
themselves and other hosts. Using bacteriophage T4, we investigated the ability of
OMVs purified from E. coli to adsorb phage as well as how this interaction affected
the efficiency of infection. We found that OMVs are protective against antimicrobial
peptides, as well as bacteriophage. In the course of understanding this protection
we also observed and characterized the cross species effects of both OMV protection
as well as phage infection. Where typically a phage infects a specific species, we
found that T4 associated OMVs treating a non-native host P. aeruginosa resulted in
the production of a novel prophage. Upon further examination, we determined that this
induction was occurring via a novel pathway that we attempted to further characterize
by performing a genetic screen to identify genes important to this induction. The
work within this dissertation fully supports the hypothesis of a regulated response
to outer membrane acting stimuli, resulting in the induction of vesiculation and the
adsorption of stressor in the extra-cellular milieu. This model of protection agrees
with the idea of a bacterial innate defense system, which acts in the short term before
the adaptive response can fully occur, resulting in a bridge between the untreated
to the treated and resistant culture.</p>
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