Apoptosis is Induced in Chlamydia trachomatis-infected HEp-2 Cells by the Addition of a Combination Innate Immune Activation Compounds and the Inhibitor Wedelolactone

Huston, Wilhelmina M.; Gloeckl, Sarina; Boer, Leonore de; Beagley, Kenneth W.

doi:10.1111/j.1600-0897.2010.00936.x

Cited by 9 publications

(7 citation statements)

References 12 publications

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“…Moreover, recent data have demonstrated that wedelolactone significantly repressed the level of phosphorylated inhibitor of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and p65 [33][34][35][36]. Here, we demonstrated that wedelolactone has antioxidative effect through inhibiting IKK activity and p65 expression by EMSA.…”

Section: Discussionmentioning

confidence: 54%

Wedelolactone protects human bronchial epithelial cell injury against cigarette smoke extract-induced oxidant stress and inflammation responses through Nrf2 pathway

Ding

Hou

Yuan

et al. 2015

International Immunopharmacology

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Section: Discussionmentioning

confidence: 54%

Wedelolactone protects human bronchial epithelial cell injury against cigarette smoke extract-induced oxidant stress and inflammation responses through Nrf2 pathway

Ding

Hou

Yuan

et al. 2015

International Immunopharmacology

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“…Ac-YVAD-CHO was used at a concentration of 10 μM (Garcia-Calvo et al, 1998), and replaced daily. Wedelolactone was used at 2 μM concentration [18]. Both PD98059 and U0126 were used at a concentration of 10 μM.…”

Section: Methodsmentioning

confidence: 99%

The IL-6 response to Chlamydia from primary reproductive epithelial cells is highly variable and may be involved in differential susceptibility to the immunopathological consequences of chlamydial infection

et al. 2013

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BackgroundChlamydia trachomatis infection results in reproductive damage in some women. The process and factors involved in this immunopathology are not well understood. This study aimed to investigate the role of primary human cellular responses to chlamydial stress response proteases and chlamydial infection to further identify the immune processes involved in serious disease sequelae.ResultsLaboratory cell cultures and primary human reproductive epithelial cultures produced IL-6 in response to chlamydial stress response proteases (CtHtrA and CtTsp), UV inactivated Chlamydia, and live Chlamydia. The magnitude of the IL-6 response varied considerably (up to 1000 pg ml-1) across different primary human reproductive cultures. Thus different levels of IL-6 production by reproductive epithelia may be a determinant in disease outcome. Interestingly, co-culture models with either THP-1 cells or autologous primary human PBMC generally resulted in increased levels of IL-6, except in the case of live Chlamydia where the level of IL-6 was decreased compared to the epithelial cell culture only, suggesting this pathway may be able to be modulated by live Chlamydia. PBMC responses to the stress response proteases (CtTsp and CtHtrA) did not significantly vary for the different participant cohorts. Therefore, these proteases may possess conserved innate PAMPs. MAP kinases appeared to be involved in this IL-6 induction from human cells. Finally, we also demonstrated that IL-6 was induced by these proteins and Chlamydia from mouse primary reproductive cell cultures (BALB/C mice) and mouse laboratory cell models.ConclusionsWe have demonstrated that IL-6 may be a key factor for the chlamydial disease outcome in humans, given that primary human reproductive epithelial cell culture showed considerable variation in IL-6 response to Chlamydia or chlamydial proteins, and that the presence of live Chlamydia (but not UV killed) during co-culture resulted in a reduced IL-6 response suggesting this response may be moderated by the presence of the organism.

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“…IL‐10 down‐regulates NO induced by other pathogens including P. brasiliensis (Moreira et al ., ) and parasites (Gazzinelli et al ., ), and macrophages deficient in IL‐10 kill C. pneumoniae better than the wild‐type macrophages, which appears to be related to iNOS (Rothfuchs et al ., ). In addition, mechanisms of host cell death, which are effected by NO in other infections (Ulett & Adderson, ), are modulated by Chlamydia in various cell types including epithelial cells, T lymphocytes, and macrophages (Yaraei et al ., ; Huston et al ., ; Olivares‐Zavaleta et al ., ). Modulation of host cell death (including inhibition of) by Chlamydia has also been linked to altered redox (Sessa et al ., ) and ROS (Vardhan et al ., ), among other mechanisms as reviewed elsewhere (Sharma & Rudel, ).…”

Section: Newly Discovered Microbial Triggers Of Il‐10 In the Hostmentioning

confidence: 99%

Recent insights into microbial triggers of interleukin-10 production in the host and the impact on infectious disease pathogenesis: Table 1

Duell

Tan

Carey

et al. 2012

FEMS Immunol Med Microbiol

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Since its initial description as a Th2-cytokine antagonistic to interferon-alpha and granulocyte-macrophage colony-stimulating factor, many studies have shown various anti-inflammatory actions of interleukin-10 (IL-10), and its role in infection as a key regulator of innate immunity. Studies have shown that IL-10 induced in response to microorganisms and their products plays a central role in shaping pathogenesis. IL-10 appears to function as both sword and shield in the response to varied groups of microorganisms in its capacity to mediate protective immunity against some organisms but increase susceptibility to other infections. The nature of IL-10 as a pleiotropic modulator of host responses to microorganisms is explained, in part, by its potent and varied effects on different immune effector cells which influence antimicrobial activity. A new understanding of how microorganisms trigger IL-10 responses is emerging, along with recent discoveries of how IL-10 produced during disease might be harnessed for better protective or therapeutic strategies. In this review, we summarize studies from the past 5 years that have reported the induction of IL-10 by different classes of pathogenic microorganisms, including protozoa, nematodes, fungi, viruses and bacteria and discuss the impact of this induction on the persistence and/or clearance of microorganisms in the host.

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Apoptosis is Induced in Chlamydia trachomatis-infected HEp-2 Cells by the Addition of a Combination Innate Immune Activation Compounds and the Inhibitor Wedelolactone

Abstract: This is the first time that induction of apoptosis has been reported in C. trachomatis-infected cells when treated with a combination of innate immune activators and wedelolactone.

Cited by 9 publications

References 12 publications

Wedelolactone protects human bronchial epithelial cell injury against cigarette smoke extract-induced oxidant stress and inflammation responses through Nrf2 pathway

Wedelolactone protects human bronchial epithelial cell injury against cigarette smoke extract-induced oxidant stress and inflammation responses through Nrf2 pathway

The IL-6 response to Chlamydia from primary reproductive epithelial cells is highly variable and may be involved in differential susceptibility to the immunopathological consequences of chlamydial infection

Recent insights into microbial triggers of interleukin-10 production in the host and the impact on infectious disease pathogenesis: Table 1

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