Identifying the role of commensal bacteria in protection against mucosal herpes simplex virus infection점막을 통한 herpes simplex 바이러스 감염에서 공생 박테리아의 역할 규명

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Commensal bacteria colonize barrier surfaces including the skin, vaginal, upper respiratory, and gastrointestinal tracts of mammals. Especially, intestinal commensals compose the largest and most diverse microbial communities. They have beneficial properties ranging from aiding in metabolism to suppressing invasive pathogens by displacing them from a microbial niche. Moreover, they play roles in immune cell development and maintaining immune homeostasis of the intestine. Recently it was reported that antiviral immunity to systemic LCMV or respiratory influenza virus infection was impaired after manipulation of intestinal commensal bacteria. However, it remains unclear whether there is a role of local resident commensals, outside the gastrointestinal tract, in shaping the antiviral immune function at nonintestinal mucosal surface. In this study, we identified the role of commensal bacteria in antiviral protection against herpes simplex virus type 2 (HSV-2) infection in vaginal mucosa. By using 4-week-antibiotics treatment, we found that mice depleted of commensal bacteria were more susceptible to intravaginal HSV-2 infection. These mice showed increased mortality and decreased viral clearance. However, in contrast to the other reports mentioned above, antibiotics-treated mice showed normal type I interferon (IFN) responses and normal T cell responses, which are main innate and adaptive immune mechanisms against HSV-2 infection, respectively. However, we revealed that IFN-$\gamma$ secretion from vaginal mucosa was severely impaired in antibiotics-treated mice due to the defective migration of effector T cells to the site of infection. IL-18, but not IL-1$\alpha$ and IL-1$\beta$, seemed to be indispensable for the protection against genital HSV-2 infection, although synthesis of all three cytokines were impaired after antibiotics treatment. Interestingly, IL-33, which suppresses the IFN-$\gamma$ production following genital HSV-2 infection, was highly expressed in vaginal mucosa after antibiotics treatment. However, it is necessary to find out a precise mechanism by which IL-33 affects the immune responses in response to the genital HSV-2 infection. Our result, collectively, demonstrate the importance of commensal microbiota in controlling the antiviral immunity in the vaginal mucosa.
Advisors
Lee, Heung Kyuresearcher이흥규researcher
Description
한국과학기술원 :의과학대학원,
Publisher
한국과학기술원
Issue Date
2014
Identifier
325007
Language
eng
Description

학위논문(박사) - 한국과학기술원 : 의과학대학원, 2014.2,[vi, 74 p. :]

Keywords

herpes simplex virus▼acommensal bacteria▼aIL-1 family cytokine▼ainterferon-gamma▼aT cell recruitment; herpes simplex 바이러스▼a공생 박테리아▼aIL-1 family 사이토카인▼ainterferon-gamma▼aT 세포 이동

URI
http://hdl.handle.net/10203/265098
Link
http://library.kaist.ac.kr/search/detail/view.do?bibCtrlNo=848995&flag=dissertation
Appears in Collection
MSE-Theses_Ph.D.(박사논문)
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