<i>Chlamydia trachomatis</i> induces lncRNA MIAT upregulation to regulate mitochondria‐mediated host cell apoptosis and chlamydial development

Luo, Feilong; Wen, Yang; Zhao, Lanhua; Su, Shengmei; Zhao, Yuqi; Lei, Wenbo; Li, Zhongyu

doi:10.1111/jcmm.17069

Cited by 8 publications

(8 citation statements)

References 65 publications

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“…Persistent C. trachomatis infection induces a host in ammatory response leading to pathological damage, and the key factor is the oversecretion of proin ammatory cytokines and chemokines (41)(42)(43). In our previous work, we conducted RNA chip sequencing for persistent infection and screened out the upregulated MAP4K4 from the differential mRNAs enriched in the in ammation signaling pathways through bioinformatics analysis (44). In addition, in antiviral studies, Emel Esen et al con rmed that MAP4K4 signi cantly inhibited the proliferation and activation of immune cells(26).…”

Section: Discussionmentioning

confidence: 99%

MAP4K4 promotes chlamydial infectivity and genital tract inflammatory injury by negatively regulating protective immunity in Chlamydia infection

Luo

2023

Preprint

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Persistent Chlamydia trachomatis infection is a risk factor for tubal infertility, and the pathology is largely due to the inflammatory response; however, the underlying molecular mechanism remains to be elucidated. MAP4K4, which has been implicated in inflammation, was upregulated in Chlamydia persistent infection in our previous study. Here, we employed both in vitro and in vivo models to evaluate the role of MAP4K4 in Chlamydia infection. We demonstrated that MAP4K4 promoted Chlamydia infectivity and increased survival in the genital tract of mice and had a palliative effect on acute inflammation. Additionally, it was beneficial to the development of chronic oviduct lesions. Mechanistically, MAP4K4 downregulated cytokine secretion, regulating the bactericidal effect of the inflammatory response. In addition, MAP4K4 negatively regulates T cell immunity by reducing the proportion of CD8+ T cells and the secretion of IFN-γ and TNF-α by T cells. Thus, these data suggest that MAP4K4 is essential in regulating the host immune response that controls Chlamydia replication, driving the inflammation that causes complications such as infertility. This work provides a novel target for adjuvant therapy of Chlamydia infection.

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Section: Discussionmentioning

confidence: 99%

MAP4K4 promotes chlamydial infectivity and genital tract inflammatory injury by negatively regulating protective immunity in Chlamydia infection

Luo

2023

Preprint

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“…Expression of many ncRNAs is altered during growth stress stimuli that induce persistent growth, particularly IFN-γ and carbenicillin [92]. Recent findings provided evidence that lncRNAs are involved in regulating apoptosis pathways in Chlamydia [93,94]. The anti-apoptotic activity of the lncRNAs includes modulation of the DNA replication and apoptosis of host cells via Wnt/β-catenin pathway [93] or downregulation of the Bcl-2/Bax ratio with a marked release of cytochrome c, resulting in a significantly elevated level of caspase-3 activation [94].…”

Section: Inhibition Of Apoptosis By Non-coding Rna'smentioning

confidence: 99%

“…Recent findings provided evidence that lncRNAs are involved in regulating apoptosis pathways in Chlamydia [93,94]. The anti-apoptotic activity of the lncRNAs includes modulation of the DNA replication and apoptosis of host cells via Wnt/β-catenin pathway [93] or downregulation of the Bcl-2/Bax ratio with a marked release of cytochrome c, resulting in a significantly elevated level of caspase-3 activation [94]. One of the Chlamydial targeted lncRNA (MIAT) was involved in regulating Chlamydial development during the persistent infection [94].…”

Section: Inhibition Of Apoptosis By Non-coding Rna'smentioning

confidence: 99%

“…The anti-apoptotic activity of the lncRNAs includes modulation of the DNA replication and apoptosis of host cells via Wnt/β-catenin pathway [93] or downregulation of the Bcl-2/Bax ratio with a marked release of cytochrome c, resulting in a significantly elevated level of caspase-3 activation [94]. One of the Chlamydial targeted lncRNA (MIAT) was involved in regulating Chlamydial development during the persistent infection [94]. The discovery of non-coding circular RNAs (circRNAs) has opened the possibility of the role of these rare RNAs in Chlamydia persistence.…”

Section: Inhibition Of Apoptosis By Non-coding Rna'smentioning

confidence: 99%

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Persistence in Chlamydia

Scharbaai-Vázquez,

J. López Font,

A. Zayas Rodríguez

2023

Infectious Diseases

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Chlamydia spp. are important causes of acute and persistent/chronic infections. All Chlamydia spp. display a unique biphasic developmental cycle alternating between an infectious elementary body (EB) and a replicative form, the reticulate body (RB), followed by the multiplication of RBs by binary fission and progressive differentiation back into EBs. During its intracellular life, Chlamydia employs multiple mechanisms to ensure its persistence inside the host. These include evasion of diverse innate immune responses, modulation of host cell structure and endocytosis, inhibition of apoptosis, activation of pro-signaling pathways, and conversion to enlarged, non-replicative but viable “aberrant bodies” (ABs). Early research described several systems for Chlamydial persistence with a significant number of variables that make a direct comparison of results difficult. Now, emerging tools for genetic manipulations in Chlamydia and advances in global microarray, transcriptomics, and proteomics have opened new and exciting opportunities to understand the persistent state of Chlamydia and link the immune and molecular events of persistence with the pathogenesis of recurrent and chronic Chlamydial infections. This chapter reviews our current understanding and advances in the molecular biology of Chlamydia persistence.

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“…The emergence of resistant C. trachomatis has determined worldwide scientists to search for novel drugs against these strains. Worryingly, recent evidence suggests the regulation of mitochondria-mediated host cell apoptosis as a survival in vivo mechanism [ 140 ]. Corallopyronin A is an antibacterial molecule synthesized by Corallococcus coralloides .…”

Section: Novel Drugs and Nano Moleculesmentioning

confidence: 99%

Fascinating Molecular and Immune Escape Mechanisms in the Treatment of STIs (Syphilis, Gonorrhea, Chlamydia, and Herpes Simplex)

Scurtu

Jinga

Simionescu

2022

IJMS

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The incidence of syphilis, gonorrhea, chlamydia, and herpes simplex has increased over the last decade, despite the numerous prevention strategies. Worldwide scientists report a surge in drug-resistant infections, particularly in immunocompromised patients. Antigenic variations in syphilis enable long-term infection, but benzathine penicillin G maintains its efficiency, whereas macrolides should be recommended with caution. Mupirocin and zoliflodacin were recently introduced as therapies against ceftriaxone-resistant gonococcus, which poses a larger global threat. The gastrointestinal and prostatic potential reservoirs of Chlamydia trachomatis may represent the key towards complete eradication. Similar to syphilis, macrolides resistance has to be considered in genital chlamydiosis. Acyclovir-resistant HSV may respond to the novel helicase-primase inhibitors and topical imiquimod, particularly in HIV-positive patients. Novel drugs can overcome these challenges while nanocarriers enhance their potency, particularly in mucosal areas. This review summarizes the most recent and valuable discoveries regarding the immunopathogenic mechanisms of these sexually transmitted infections and discusses the challenges and opportunities of the novel molecules and nanomaterials.

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Chlamydia trachomatis induces lncRNA MIAT upregulation to regulate mitochondria‐mediated host cell apoptosis and chlamydial development

Cited by 8 publications

References 65 publications

MAP4K4 promotes chlamydial infectivity and genital tract inflammatory injury by negatively regulating protective immunity in Chlamydia infection

MAP4K4 promotes chlamydial infectivity and genital tract inflammatory injury by negatively regulating protective immunity in Chlamydia infection

Persistence in Chlamydia

Fascinating Molecular and Immune Escape Mechanisms in the Treatment of STIs (Syphilis, Gonorrhea, Chlamydia, and Herpes Simplex)

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