<i>Chlamydia psittaci</i>
            -Infected Dendritic Cells Communicate with NK Cells via Exosomes To Activate Antibacterial Immunity

Radomski, Nadine; Karger, Axel; Franzke, Kati; Liebler-Tenorio, Elisabeth M.; Jahnke, Rico; Matthiesen, Svea; Knittler, Michael R.

doi:10.1128/iai.00541-19

Cited by 18 publications

(25 citation statements)

References 96 publications

(111 reference statements)

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“…First, TNF-a works with IFN-g to inhibits the metabolism of host cells by increasing the activity of indoleamine 2, 3-dioxygenase (IDO), and restricts the growth of Chlamydia (36,56). Secondly, TNF-a influences the survival of Chlamydia in vivo by inducing apoptosis of host cells that provide suitable conditions for the growth of the organism (57)(58)(59). Furthermore, the adoptive transfer of TNF-a reduces the lung bacterial load of newborn mice infected with Chlamydia.…”

Section: Tnfmentioning

confidence: 99%

Insights Into Host Cell Cytokines in Chlamydia Infection

Xiang

Lei

et al. 2021

Front. Immunol.

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Chlamydial infection causes a number of clinically relevant diseases and induces significant morbidity in humans. Immune and inflammatory responses contribute to both the clearance of Chlamydia infection and pathology in host tissues. Chlamydia infection stimulates host cells to produce a large number of cytokines that trigger and regulate host immune responses against Chlamydia. However, inappropriate responses can occur with excessive production of cytokines, resulting in overreactive inflammatory responses and alterations in host or Chlamydia metabolism. As a result, Chlamydia persists and causes wound healing delays, leading to more severe tissue damage and triggering long-lasting fibrotic sequelae. Here, we summarize the roles of cytokines in Chlamydia infection and pathogenesis, thus advancing our understanding chlamydial infection biology and the pathogenic mechanisms involved.

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Section: Tnfmentioning

confidence: 99%

Insights Into Host Cell Cytokines in Chlamydia Infection

Xiang

Lei

et al. 2021

Front. Immunol.

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“…Through Toll-like receptor activation in response to pathogen-derived microbial products, DC and NK cells interact, resulting in NK activation and DC maturation [1]. In an in vitro model of Chlamydia psittaci infection, activation of NK cells and strong IFN-γ production may occur also by release of exosomes from infected DC [2].…”

Section: Introductionmentioning

confidence: 99%

Production of IFN-γ by splenic dendritic cells during innate immune responses against Francisella tularensis LVS depends on MyD88, but not TLR2, TLR4, or TLR9

et al. 2020

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Production of IFN-γ is a key innate immune mechanism that limits replication of intracellular bacteria such as Francisella tularensis (Ft) until adaptive immune responses develop. Previously, we demonstrated that the host cell types responsible for IFN-γ production in response to murine Francisella infection include not only natural killer (NK) and T cells, but also a variety of myeloid cells. However, production of IFN-γ by mouse dendritic cells (DC) is controversial. Here, we directly demonstrated substantial production of IFN-γ by DC, as well as hybrid NK-DC, from LVS-infected wild type C57BL/6 or Rag1 knockout mice. We demonstrated that the numbers of conventional DC producing IFN-γ increased progressively over the course of 8 days of LVS infection. In contrast, the numbers of conventional NK cells producing IFN-γ, which represented about 40% of non-B/T IFN-γ-producing cells, peaked at day 4 after LVS infection and declined thereafter. This pattern was similar to that of hybrid NK-DC. To further confirm IFN-γ production by infected cells, DC and neutrophils were sorted from naïve and LVS-infected mice and analyzed for gene expression. Quantification of LVS by PCR revealed the presence of Ft DNA not only in macrophages, but also in highly purified, IFN-γ producing DC and neutrophils. Finally, production of IFN-γ by infected DC was confirmed by immunohistochemistry and confocal microscopy. Notably, IFN-γ production patterns similar to those in wild type mice were observed in cells derived from LVSinfected TLR2, TLR4, and TLR2xTLR9 knockout (KO) mice, but not from MyD88 KO mice. Taken together, these studies demonstrate the pivotal roles of DC and MyD88 in IFN-γ production and in initiating innate immune responses to this intracellular bacterium.

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“…Dutow et al elucidated the role of effector of the complement (C3a) in C. psittaci 02DC15 infection ( 22 ). Most recently, Radomski et al reported that C. psittaci 02DC15 infection of dendritic cells enhances exosome release, resulting in strong induction of IFN-γ production by natural killer cells and enhancement of apoptosis ( 24 ). Therefore, successful transformation using C. psittaci 02DC15 is particularly meaningful with respect to the biology of C. psittaci infection.…”

Section: Discussionmentioning

confidence: 99%

“…S8), we were able to show that all of the genes present in C. psittaci 6BC are encountered in C. psittaci 02DC15 as well, thus indicating their genetic equivalence. Due to the genome similarity between C. psittaci 6BC and C. psittaci 02DC15, C. psittaci 02DC15 is widely used for a number of immunological and cell biological studies, as well as animal infection trials (22)(23)(24)(25)(26)(27)(28). Reinhold et al established a bovine respiratory model of acute C. psittaci infection using strain 02DC15 (27).…”

Section: Figmentioning

confidence: 99%

Development of a Plasmid Shuttle Vector System for Genetic Manipulation of Chlamydia psittaci

Shima

Weber

Schnee

et al. 2020

mSphere

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The obligate intracellular bacterium Chlamydia psittaci is a known avian pathogen causing psittacosis in birds and is capable of zoonotic transmission. In human pulmonary infections, C. psittaci can cause pneumonia associated with significant mortality if inadequately diagnosed and treated. Although intracellular C. psittaci manipulates host cell organelles for its replication and survival, it has been difficult to demonstrate host-pathogen interactions in C. psittaci infection due to the lack of easy-to-handle genetic manipulation tools. Here, we show the genetic transformation of C. psittaci using a plasmid shuttle vector that contains a controllable gene induction system. The 7,553-bp plasmid p01DC12 was prepared from the nonavian C. psittaci strain 01DC12. We constructed the shuttle vector pCps-Tet-mCherry using the full sequence of p01DC12 and the 4,449-bp fragment of Chlamydia trachomatis shuttle vector pBOMB4-Tet-mCherry. pCps-Tet-mCherry includes genes encoding the green fluorescent protein (GFP), mCherry, and ampicillin resistance (AmpR). Target genes can be inserted at a multiple cloning site (MCS). Importantly, these genes can be regulated by a tetracycline-inducible (tet) promoter. Using the pCps-Tet-mCherry plasmid shuttle vector, we show the expression of GFP, as well as the induction of mCherry expression, in C. psittaci strain 02DC15, which belongs to the avian C. psittaci 6BC clade. Furthermore, we demonstrated that pCps-Tet-mCherry was stably retained in C. psittaci transformants. Thus, our C. psittaci plasmid shuttle vector system represents a novel targeted approach that enables the elucidation of host-pathogen interactions. IMPORTANCE Psittacosis, caused by avian C. psittaci, has a major economic impact in the poultry industry worldwide and represents a significant risk for zoonotic transmission to humans. In the past decade, the tools of genetic manipulation have been improved for chlamydial molecular studies. While several genetic tools have been mainly developed in Chlamydia trachomatis, a stable gene-inducible shuttle vector system has not to date been available for C. psittaci. In this study, we adapted a C. trachomatis plasmid shuttle vector system to C. psittaci. We constructed a C. psittaci plasmid backbone shuttle vector called pCps-Tet-mCherry. The construct expresses GFP in C. psittaci. Importantly, exogeneous genes can be inserted at an MCS and are regulated by a tet promoter. The application of the pCps-Tet-mCherry shuttle vector system enables a promising new approach to investigate unknown gene functions of this pathogen.

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Chlamydia psittaci -Infected Dendritic Cells Communicate with NK Cells via Exosomes To Activate Antibacterial Immunity

Cited by 18 publications

References 96 publications

Insights Into Host Cell Cytokines in Chlamydia Infection

Insights Into Host Cell Cytokines in Chlamydia Infection

Production of IFN-γ by splenic dendritic cells during innate immune responses against Francisella tularensis LVS depends on MyD88, but not TLR2, TLR4, or TLR9

Development of a Plasmid Shuttle Vector System for Genetic Manipulation of Chlamydia psittaci

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