<i>Chlamydia trachomatis</i>Cell-to-Cell Spread through Tunneling Nanotubes

Jahnke, Rico; Matthiesen, Svea; Zaeck, Luca M.; Finke, Stefan; Knittler, Michael R.

doi:10.1128/spectrum.02817-22

Cited by 10 publications

(9 citation statements)

References 84 publications

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“…Intrigued by the induction of the formation of these B cell protrusions by the parasite, we set out to investigate whether these amastigote-induced protrusions could serve any functional purpose. Previous studies have demonstrated TNTs and TNT-like protrusions formed by other cell types to be exploited for disease propagation by bacteria ( 21 – 23 ) and viruses ( 24 – 26 ), so we wanted to know whether these protrusions could be used by L. donovani to pass between cells and hence propagate activation. Indeed, we frequently observed the presence of L. donovani amastigotes on the protrusions formed between two B cells ( Fig.…”

Section: Resultsmentioning

confidence: 99%

“…These B cell TNTs were shown to enable the transport of plasma membrane proteins on the outside of the tubules as well as to allow passage of microvesicles through the inside of the tubules ( 39 , 41 ). In other cell types, previous studies have demonstrated these tubules to be exploited for disease propagation by bacteria, including Listeria monocytogenes ( 21 ), Mycobacterium bovis ( 22 ), and Chlamydia trachomatis ( 23 ), and viruses, such as HIV-1 ( 24 ), influenza A virus ( 25 ), and SARS-CoV-2 ( 26 ). Thus, the involvement of these TNT-like protrusions in the dissemination of L. donovani among B cells represents the first report of this mechanism of intercellular communication in the context of a parasitic infection.…”

Section: Discussionmentioning

confidence: 99%

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Leishmania donovani Exploits Tunneling Nanotubes for Dissemination and Propagation of B Cell Activation

et al. 2023

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Leishmania donovani is a causative agent of visceral leishmaniasis, a potentially lethal disease characterized by strong B cell activation and the subsequent excessive production of nonprotective antibodies, which are known to worsen the disease. How Leishmania activates B cells is still unknown, particularly because this parasite mostly resides inside macrophages and would not have access to B cells during infection.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Leishmania donovani Exploits Tunneling Nanotubes for Dissemination and Propagation of B Cell Activation

et al. 2023

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“…Analogous to viruses, previous work has shown that C.t. may spread cell-to-cell by nanotubules 69 . Thus, it is conceivable that effector proteins may also be transmitted to adjacent cells via this mechanism.…”

Section: Discussionmentioning

confidence: 99%

Global mapping of theChlamydia trachomatisconventional secreted effector – host interactome reveals CebN interacts with nucleoporins and Rae1 to impede STAT1 nuclear translocation

Steiert,

Andersen,

McCaslin

et al. 2024

Preprint

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Chlamydia trachomatis (C.t.), the leading cause of bacterial sexually transmitted infections, employs a type III secretion system (T3SS) to translocate two classes of effectors, inclusion membrane proteins and conventional T3SS (cT3SS) effectors, into the host cell to counter host defense mechanisms. Here we employed three assays to directly evaluate secretion during infection, validating secretion for 23 cT3SS effectors. As bioinformatic analyses have been largely unrevealing, we conducted affinity purification-mass spectrometry to identify host targets and gain insights into the functions of these effectors, identifying high confidence interacting partners for 21 cT3SS effectors. We demonstrate that CebN localizes to the nuclear envelope in infected and bystander cells where it interacts with multiple nucleoporins and Rae1, blocking STAT1 nuclear import following IFN-γ stimulation. By building a cT3SS effector-host interactome, we have identified novel pathways that are targeted during bacterial infection and have begun to address how C.t. effectors combat cell autonomous immunity.

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“…It interferes with the antigen-presenting function of antigen-presenting cells (APCs) (downregulation of MHC class I and II molecules) ( 54 , 55 ), regulating specific cytokines with multiple effects (IL-18, IFN-γ, TNF-α), and anti-apoptosis (increased cell survival signaling and CPAF release) ( 56 – 58 ). In addition, recent studies have shown that intracellular RBs can enter uninfected neighboring cells via tunneling nanotubes (TNT) ( 59 ). This allows Chlamydia to remain unexposed to body fluids, thus evading to some extent the pursuit of various cytokines in body fluids.…”

Section: Pathogenesis and Immunitymentioning

confidence: 99%

Insights into innate immune cell evasion by Chlamydia trachomatis

Wang,

Wu,

Fang

et al. 2024

Front. Immunol.

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Chlamydia trachomatis, is a kind of obligate intracellular pathogen. The removal of C. trachomatis relies primarily on specific cellular immunity. It is currently considered that CD4+ Th1 cytokine responses are the major protective immunity against C. trachomatis infection and reinfection rather than CD8+ T cells. The non-specific immunity (innate immunity) also plays an important role in the infection process. To survive inside the cells, the first process that C. trachomatis faces is the innate immune response. As the “sentry” of the body, mast cells attempt to engulf and remove C. trachomatis. Dendritic cells present antigen of C. trachomatis to the “commanders” (T cells) through MHC-I and MHC-II. IFN-γ produced by activated T cells and natural killer cells (NK) further activates macrophages. They form the body’s “combat troops” and produce immunity against C. trachomatis in the tissues and blood. In addition, the role of eosinophils, basophils, innate lymphoid cells (ILCs), natural killer T (NKT) cells, γδT cells and B-1 cells should not be underestimated in the infection of C. trachomatis. The protective role of innate immunity is insufficient, and sexually transmitted diseases (STDs) caused by C. trachomatis infections tend to be insidious and recalcitrant. As a consequence, C. trachomatis has developed a unique evasion mechanism that triggers inflammatory immunopathology and acts as a bridge to protective to pathological adaptive immunity. This review focuses on the recent advances in how C. trachomatis evades various innate immune cells, which contributes to vaccine development and our understanding of the pathophysiologic consequences of C. trachomatis infection.

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Chlamydia trachomatisCell-to-Cell Spread through Tunneling Nanotubes

Abstract: Intracellular bacterial pathogens often undergo a life cycle in which they parasitize infected host cells in membranous vacuoles. Two pathways have been described by which chlamydia can exit infected host cells: lytic cell destruction or exit via extrusion formation.

Cited by 10 publications

References 84 publications

Leishmania donovani Exploits Tunneling Nanotubes for Dissemination and Propagation of B Cell Activation

Leishmania donovani Exploits Tunneling Nanotubes for Dissemination and Propagation of B Cell Activation

Global mapping of theChlamydia trachomatisconventional secreted effector – host interactome reveals CebN interacts with nucleoporins and Rae1 to impede STAT1 nuclear translocation

Insights into innate immune cell evasion by Chlamydia trachomatis

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