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The role of lung epithelial IL-17RC signaling during influenza, MRSA, and influenza-MRSA super-infection

Marinelli, Michael (2020) The role of lung epithelial IL-17RC signaling during influenza, MRSA, and influenza-MRSA super-infection. Undergraduate Thesis, University of Pittsburgh. (Unpublished)

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Influenza is a common cause of respiratory illness contributing significantly to morbidity and mortality each year. Secondary-bacterial infections following influenza illness are less common but increase the likelihood of developing severe infection complications further increasing morbidity and mortality. IL-17, an immune system signaling molecule, induces cell signaling that drives proinflammatory activation of the immune response including the recruitment of immune cells to infection sites and inducing changes in gene expression. These actions have been shown to increase morbidity associated with influenza infections by increasing damage to host tissues. During bacterial infections, such as methicillin-resistant Staphylococcus aureus (MRSA), IL-17 signaling helps with bacterial clearance, reducing morbidity. Understanding the roles IL-17 signaling has in the lungs during different infections can help provide new avenues for therapeutic interventions. IL-17 is thought to activate immunity via signaling through its receptor on lung epithelial cells. Club cells of the lung epithelium, identified by club cell secretory protein, are known as immune activators. In this study, we sought to understand what effects IL-17 signaling in club cells has using three infection models: primary influenza, primary MRSA, and influenza-MRSA super-infection of the lungs. Mice were generated using cre-lox recombination to remove the gene for IL-17RC, a receptor subunit needed for IL-17 signaling initiation, specifically in club cells. In all three infections, no significant changes were observed between the knockouts and control mice. This suggests that IL-17A and IL-F signaling in club cells does not greatly affect the immune response in this setting.


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Item Type: University of Pittsburgh ETD
Status: Unpublished
CreatorsEmailPitt UsernameORCID
Marinelli, MichaelMAM637@pitt.eduMAM637
ETD Committee:
TitleMemberEmail AddressPitt UsernameORCID
Committee ChairAlcorn, Johnjfa9@pitt.edujfa9
Committee MemberBoyle, Jonboylej@pitt.eduboylej
Committee MemberStephenson, Jessicajess.stephenson@pitt.edujfs61
Committee MemberPociask,
Date: 4 May 2020
Date Type: Publication
Defense Date: 7 April 2020
Approval Date: 4 May 2020
Submission Date: 16 April 2020
Access Restriction: No restriction; Release the ETD for access worldwide immediately.
Number of Pages: 95
Institution: University of Pittsburgh
Schools and Programs: David C. Frederick Honors College
Dietrich School of Arts and Sciences > Biological Sciences
Degree: BPhil - Bachelor of Philosophy
Thesis Type: Undergraduate Thesis
Refereed: Yes
Uncontrolled Keywords: Inflammation, Pneumonia, Host Defense, Immunity
Date Deposited: 04 May 2020 14:07
Last Modified: 04 May 2020 14:07


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