The Role of IL-17A as a Potential Mediator of Chlamydial Pathogenesis

dc.contributor.advisorArulanandam, Bernard P.
dc.contributor.authorArkatkar, Tanvi
dc.contributor.committeeMemberGuentzel, Neal
dc.contributor.committeeMemberChambers, James
dc.date.accessioned2024-01-26T16:48:26Z
dc.date.available2024-01-26T16:48:26Z
dc.date.issued2014
dc.descriptionThis item is available only to currently enrolled UTSA students, faculty or staff. To download, navigate to Log In in the top right-hand corner of this screen, then select Log in with my UTSA ID.
dc.description.abstractPURPOSE: IL-17 has been reported to play an important role in host defenses against pulmonary chlamydial infections by promoting a Th1 response. However, molecular mechanisms associated with IL-17 in genital chlamydial infection have not been well characterized and were the purpose of this study. METHODS: C57BL/6 wild type (WT) and IL-17-/- mice were intravaginally challenged with C. muridarum (CM) and differences in infiltrating lymphocytes, T and B cell responses and miRNA expression were analyzed. We isolated RNA from the lower genital tracts of CM infected WT and IL-17A-/- mice and analyzed the gene transcripts with a high throughput qPCR based array for 84 genes associated with T and B cell activation. RESULTS: Pathology was decreased at day 80 post challenge in IL-17A-/- compared to WT mice. Six genes were significantly (p<0.05) regulated at day 6 post-challenge including ICAM1 and IL-1&#946; which are known mediators of pathology. These genes were further analyzed (miRNA based in silico prediction software); miRNA 214 was significantly upregulated in IL-17-/- mice, which has two target binding sites for the downregulated ICAM-1 gene. Additionally, we derived miR 214 over expressing genital cells which decreased ICAM-1 with CM infection in vitro. Furthermore, recruitment of neutrophils in IL-17 A-/- was reduced compared to WT mice. CONCLUSION: Decreased pathology in IL-17 A-/- mice may be attributed to reduced expression of ICAM-1 leading to reduction in neutrophil infiltration at the early stage of genital infection.
dc.description.departmentIntegrative Biology
dc.format.extent34 pages
dc.format.mimetypeapplication/pdf
dc.identifier.urihttps://hdl.handle.net/20.500.12588/2543
dc.languageen
dc.subject.classificationImmunology
dc.titleThe Role of IL-17A as a Potential Mediator of Chlamydial Pathogenesis
dc.typeThesis
dc.type.dcmiText
dcterms.accessRightspq_closed
thesis.degree.departmentIntegrative Biology
thesis.degree.grantorUniversity of Texas at San Antonio
thesis.degree.levelMasters
thesis.degree.nameMaster of Science

Files

Original bundle

Now showing 1 - 1 of 1
No Thumbnail Available
Name:
Arkatkar_utsa_1283M_11438.pdf
Size:
612.91 KB
Format:
Adobe Portable Document Format