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Comparative analysis of chlamydia infection in wild type mice and mice with epithelial autophagy deficiency

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TitleInfo
Title
Comparative analysis of chlamydia infection in wild type mice and mice with epithelial autophagy deficiency
Name (type = personal)
NamePart (type = family)
Battaglia
NamePart (type = given)
Lauren
NamePart (type = date)
1988-
DisplayForm
Lauren Battaglia
Role
RoleTerm (authority = RULIB)
author
Name (type = personal)
NamePart (type = family)
Fan
NamePart (type = given)
Huizhou
DisplayForm
Huizhou Fan
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
chair
Name (type = personal)
NamePart (type = family)
Jacinto
NamePart (type = given)
Estela
DisplayForm
Estela Jacinto
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
internal member
Name (type = personal)
NamePart (type = family)
Haimovich
NamePart (type = given)
Beatrice
DisplayForm
Beatrice Haimovich
Affiliation
Advisory Committee
Role
RoleTerm (authority = RULIB)
outside member
Name (type = corporate)
NamePart
Rutgers University
Role
RoleTerm (authority = RULIB)
degree grantor
Name (type = corporate)
NamePart
Graduate School - New Brunswick
Role
RoleTerm (authority = RULIB)
school
TypeOfResource
Text
Genre (authority = marcgt)
theses
OriginInfo
DateCreated (qualifier = exact)
2013
DateOther (qualifier = exact); (type = degree)
2013-10
Place
PlaceTerm (type = code)
xx
Language
LanguageTerm (authority = ISO639-2b); (type = code)
eng
Abstract (type = abstract)
Chlamydia is the most common cause of sexually transmitted bacterial infection worldwide and it leads to severe complications for women who become infected. Following initial infection, the bacterial pathogen ascends from the lower genital tract to the upper genital tract leading to pelvic inflammation and scarring of inflamed tissue. The scarring can lead to ductal obstruction, causing retention of fluid in the upper genital tract and ovaries, termed hydrosalpinx. This inflammation due to Chlamydia infection can lead to infertility. Despite the commonality of the disease and its severe consequences, the molecular pathogenesis and mechanism of pelvic inflammation following Chlamydia infection has yet to be elucidated. We investigated the molecular pathogenesis and its relation to host autophagy here. The ATG5 gene is required for autophagy. Our lab has previously shown via mouse model that deletion of the ATG5 gene in myeloid cells results in a significant increase in upper genital tract inflammation following Chlamydia infection. To further investigate the role of autophagy in Chlamydia pathogenesis, mice with deleted ATG5 gene in epithelial cells were intravaginally infected with Chlamydia. The infection was monitored through weekly vaginal swabbing and calculation of Chlamydia bacterial titers from each swab. After Chlamydia infection cleared, the animals were sacrificed, upper genital tract pathology was observed and cytokine analysis was conducted on the vaginal swabs that were taken throughout the infection. The p62 autophagy protein acts as a scaffold to bring bacterial pathogen to autophagy machinery. In the current study, p62-deficient mice were obtained and infected with Chlamydia. Vaginal swabbing throughout Chlamydia infection allowed us to estimate bacterial titers and assay the host cytokine response to the infection, and finally the upper genital tracts of the animals were removed for observation. We found no significant difference in the pathology, bacterial clearance, or cytokine analysis between epithelial Atg5-deficient animals and wild type animals. This suggests that the Chlamydia bacteria may be employing mechanisms to evade or inhibit host autophagy in epithelial cells to promote its own survival. Additionally, there was no significant difference in the pathology, bacterial clearance, or cytokine analysis between the p62-deficient animals and wild type animals.
Subject (authority = RUETD)
Topic
Cell and Developmental Biology
RelatedItem (type = host)
TitleInfo
Title
Rutgers University Electronic Theses and Dissertations
Identifier (type = RULIB)
ETD
Identifier
ETD_4889
PhysicalDescription
Form (authority = gmd)
electronic resource
InternetMediaType
application/pdf
InternetMediaType
text/xml
Extent
viii, 68 p. : ill.
Note (type = degree)
M.A.
Note (type = bibliography)
Includes bibliographical references
Note (type = statement of responsibility)
by Lauren Battaglia
Subject (authority = ETD-LCSH)
Topic
Chlamydia infections in animals
Subject (authority = ETD-LCSH)
Topic
Chlamydia
Subject (authority = ETD-LCSH)
Topic
Generative organs, Female--Diseases
RelatedItem (type = host)
TitleInfo
Title
Graduate School - New Brunswick Electronic Theses and Dissertations
Identifier (type = local)
rucore19991600001
Location
PhysicalLocation (authority = marcorg); (displayLabel = Rutgers, The State University of New Jersey)
NjNbRU
Identifier (type = doi)
doi:10.7282/T3ZK5DPG
Genre (authority = ExL-Esploro)
ETD graduate
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Rights

RightsDeclaration (ID = rulibRdec0006)
The author owns the copyright to this work.
RightsHolder (type = personal)
Name
FamilyName
Battaglia
GivenName
Lauren
Role
Copyright Holder
RightsEvent
Type
Permission or license
DateTime (encoding = w3cdtf); (qualifier = exact); (point = start)
2013-06-20 21:25:43
AssociatedEntity
Name
Lauren Battaglia
Role
Copyright holder
Affiliation
Rutgers University. Graduate School - New Brunswick
AssociatedObject
Type
License
Name
Author Agreement License
Detail
I hereby grant to the Rutgers University Libraries and to my school the non-exclusive right to archive, reproduce and distribute my thesis or dissertation, in whole or in part, and/or my abstract, in whole or in part, in and from an electronic format, subject to the release date subsequently stipulated in this submittal form and approved by my school. I represent and stipulate that the thesis or dissertation and its abstract are my original work, that they do not infringe or violate any rights of others, and that I make these grants as the sole owner of the rights to my thesis or dissertation and its abstract. I represent that I have obtained written permissions, when necessary, from the owner(s) of each third party copyrighted matter to be included in my thesis or dissertation and will supply copies of such upon request by my school. I acknowledge that RU ETD and my school will not distribute my thesis or dissertation or its abstract if, in their reasonable judgment, they believe all such rights have not been secured. I acknowledge that I retain ownership rights to the copyright of my work. I also retain the right to use all or part of this thesis or dissertation in future works, such as articles or books.
Copyright
Status
Copyright protected
Availability
Status
Open
Reason
Permission or license
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Technical

RULTechMD (ID = TECHNICAL1)
ContentModel
ETD
OperatingSystem (VERSION = 5.1)
windows xp
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