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INTERLEUKIN-10 AS A NEGATIVE REGULATOR OF INTERFERON-MEDIATED IMMUNITY IN CHLAMYDIAL INFECTIONS

Jung, Joo-Yong
http://rave.ohiolink.edu/etdc/view?acc_num=miami1196971379

Abstract Details

2007, Doctor of Philosophy, Miami University, Microbiology.
IFN-induced indoleamine 2,3-dioxygenase (IDO) inhibits intracellular chlamydiae by restricting the availability of tryptophan required for chlamydial growth. The pro-inflammatory cytokines that synergistically enhance IDO activity, IL-1β and TNF-α, are produced by macrophages during in vitro chlamydial infections. These cytokines may be involved in the intensive inflammatory responses at sites of infection. However, asymptomatic infection occurs in 70-90% of infected patients, suggesting that antagonistic cytokines might be generated during the immune response in vivo. Interleukin-10 is an anti-inflammatory cytokine with potent immunomodulatory effects, including the inhibition of cytokine production. If IL-10 is produced during a chlamydial infection, it might inhibit the production of pro-inflammatory cytokines capable of up-regulating anti-chlamydial IDO activity. The purpose of this study was to evaluate the effectiveness of IL-10 production as a mechanism by which chlamydiae evade the effects of IFN-γ. It was found that IL-10 treatment of macrophage cultures inhibited the production of IFN-α, IL-1β and TNF α as well as the induction of IDO activity in response to chlamydial infection in a concentration-related manner. IL-1β and TNF-α were detected by 24 h after exposure to UV-inactivated Chlamydophila psittaci and live Chlamydia trachomatis, whereas IL-10 was detected at approximately 48 h after exposure to chlamydiae. The mechanism of IL-10 production in response to chlamydial infection was explored. It was found that IL-10 production from macrophages exposed to chlamydiae was dependent upon endogenous production of IL-1β and TNF-α. Since UV-inactivated C. psittaci and C. trachomatis were unable to replicate in macrophages, involvement of chlamydiae-Toll like receptor 2 (TLR2) and 4 (TLR4) interaction on IL-1β and TNF-α production was explored. Endogenous production of IL-1β and TNF-α were initiated following the interaction between Chlamydia and TLR2 and TLR4 on the surface of macrophages. These results indicate that Chlamydia-TLR interaction stimulates a cascade of cytokine production capable of either up-regulating or down-regulating IFN γ-induced IDO activity. Overall this study suggests that IL-10 produced following Chlamydia-TLR interaction may inhibit the induction of effective immunological responses by inhibiting pro-inflammatory cytokine production by macrophages.
Joseph Carlin (Advisor)
178 p.
Biology, Microbiology
Chlamydia, IL-1&946; , TNF-&945; , macrophages, IL-10, IFN-&947; ,indoleamine 2,3-dioxygenase (IDO)

Recommended Citations

Citations

  • Jung, J.-Y. (2007). INTERLEUKIN-10 AS A NEGATIVE REGULATOR OF INTERFERON-MEDIATED IMMUNITY IN CHLAMYDIAL INFECTIONS [Doctoral dissertation, Miami University]. OhioLINK Electronic Theses and Dissertations Center. http://rave.ohiolink.edu/etdc/view?acc_num=miami1196971379

    APA Style (7th edition)

  • Jung, Joo-Yong. INTERLEUKIN-10 AS A NEGATIVE REGULATOR OF INTERFERON-MEDIATED IMMUNITY IN CHLAMYDIAL INFECTIONS. 2007. Miami University, Doctoral dissertation. OhioLINK Electronic Theses and Dissertations Center, http://rave.ohiolink.edu/etdc/view?acc_num=miami1196971379.

    MLA Style (8th edition)

  • Jung, Joo-Yong. "INTERLEUKIN-10 AS A NEGATIVE REGULATOR OF INTERFERON-MEDIATED IMMUNITY IN CHLAMYDIAL INFECTIONS." Doctoral dissertation, Miami University, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=miami1196971379

    Chicago Manual of Style (17th edition)

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This open access ETD is published by Miami University and OhioLINK.