Mode of Entry and Release of Chlamydiae in Infections of Intestinal Epithelial Cells

Doughri, A.M.; Storz, J.; tera, K P A

doi:10.1093/infdis/126.6.652

Cited by 42 publications

(38 citation statements)

References 7 publications

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“…Thus, we envision that the released, inclusion-containing epithelial cell would act like a chlamydial 'cluster bomb', allowing delivery of a concentrated inoculum over a relatively long distance and increasing the possibility of a 'hit' if the host cell ruptured near the genital epithelial cell layer. Interestingly, release of intact, chlamydiae-infected host cells from polarized monolayers in culture (Wyrick et al, 1989) as well as from infected epithelium in vivo has been observed (Doughri et al, 1972;Soloff et al, 1985). Of course, it is always possible that the observed nectin-1 decrease is an indirect side-effect of other host cytoskeletal or physiological alterations induced during chlamydial infection.…”

Section: Discussionmentioning

confidence: 99%

“…This cell-cell disassociation was later shown to be due, at least in part, to disruption of N-cadherin-dependent cell-cell junctions and breakdown of the N-cadherin/b-catenin complex (Prozialeck et al, 2002). Notably, infected epithelial cell release has also been observed in vivo (Doughri et al, 1972;Soloff et al, 1985). Doughri et al (1972) further suggested that release of chlamydiae within intact host cells might protect the organisms from anti-chlamydial antibodies.…”

Section: Introductionmentioning

confidence: 94%

“…Notably, infected epithelial cell release has also been observed in vivo (Doughri et al, 1972;Soloff et al, 1985). Doughri et al (1972) further suggested that release of chlamydiae within intact host cells might protect the organisms from anti-chlamydial antibodies. In both studies, the authors hypothesize that polymorphonuclear neutrophils (PMNs) responding to chlamydial infection promote detachment of chlamydia-infected cells from the mucosal surface, resulting in the release of intact, infected cells into the cervical lumen (Doughri et al, 1972;Soloff et al, 1985).…”

Section: Introductionmentioning

confidence: 94%

“…Doughri et al (1972) further suggested that release of chlamydiae within intact host cells might protect the organisms from anti-chlamydial antibodies. In both studies, the authors hypothesize that polymorphonuclear neutrophils (PMNs) responding to chlamydial infection promote detachment of chlamydia-infected cells from the mucosal surface, resulting in the release of intact, infected cells into the cervical lumen (Doughri et al, 1972;Soloff et al, 1985). The seminal observation that chlamydial infection in the absence of PMNs loosens cell-cell junctions by promoting breakdown of the N-cadherin/b-catenin complex (Prozialeck et al, 2002) suggests that the developing chlamydiae may also contribute directly to the release observed in vivo of infected cells from the infected mucosa.…”

Section: Introductionmentioning

confidence: 99%

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The host adherens junction molecule nectin-1 is downregulated in Chlamydia trachomatis-infected genital epithelial cells

2008

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The host adherens junction molecule nectin-1 is downregulated in Chlamydia trachomatis-infected genital epithelial cells

2008

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“…This is a controlled process dependent on both bacterial and host factors, which leaves the host cell intact and often residually infected (14,17). The role of extrusion during human infection is unknown, but it occurs in approximately 50% of infected cells in vitro and has been observed in an animal model of in vivo infection (14,17,18). The potential infectious advantages of extrusion for immune evasion, bacterial survival, and dissemination are striking.…”

mentioning

confidence: 99%

Chlamydia trachomatis Cellular Exit Alters Interactions with Host Dendritic Cells

Sherrid

Hybiske

2017

Infect Immun

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The strategies utilized by pathogens to exit host cells are an area of pathogenesis which has received surprisingly little attention, considering the necessity of this step for infections to propagate. Even less is known about how exit through these pathways affects downstream host-pathogen interactions and the generation of an immune response. Chlamydia trachomatis exits host epithelial cells through two equally active mechanisms: lysis and extrusion. Studies have characterized the outcome of interactions between host innate immune cells, such as dendritic cells and macrophages, and free, extracellular Chlamydia bacteria, such as those resulting from lysis. Exit via extrusion generates a distinct, host-membranebound compartment of Chlamydia separate from the original infected cell. In this study, we assessed the effect of containment within extrusions upon the interaction between Chlamydia and host dendritic cells. Extrusion dramatically affected the outcome of Chlamydia-dendritic cell interactions for both the bacterium and the host cell. Dendritic cells rapidly underwent apoptosis in response to engulfment of an extrusion, while uptake of an equivalent dose of free Chlamydia had no such effect. Containment within an extrusion also prolonged bacterial survival within dendritic cells and altered the initial innate immune signaling by the dendritic cell.KEYWORDS Chlamydia, apoptosis, dendritic cell, extrusion C hlamydia trachomatis is a highly successful Gram-negative bacterial pathogen, being the leading bacterial cause of sexually transmitted infections and the leading cause of infectious blindness globally (1-3). In the absence of diagnosis and treatment, Chlamydia infections can lead to severe long-term outcomes, such as chronic pelvic pain, infertility, and ectopic pregnancy (4, 5). During infection, innate and adaptive immune responses are mounted against Chlamydia; however, approximately 50% of infections last for a year or more (6). Even after the resolution of infection, only partial protective immunity is achieved and reinfection is common (7-9). This suggests that Chlamydia is adept at establishing and sustaining infection in the face of immune recognition.Due to Chlamydia's obligate intracellular nature and a historically limited genetic toolbox, key attributes of the host-Chlamydia interaction are still unknown. Chlamydia infection is initiated by the uptake of metabolically inactive elementary bodies (EB) into mucosal epithelial cells, which transition into reticulate bodies (RB) within a vacuole called an inclusion. Here, the metabolically active RB replicates robustly to generate hundreds of Chlamydia bacteria that undergo transition back to EB (10). Chlamydia inhibits apoptosis of the host epithelial cell, ensuring its ability to complete this replication cycle before exit from the cell (11-13). Bacterial exit from host cells is a crucial but underscrutinized stage of the life cycle of this and other intracellular pathogens. Chlamydia possesses two distinct, equally prevalent exit mechan...

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Optimal development of Chlamydophila psittaci in L929 fibroblast and BGM epithelial cells requires the participation of microfilaments and microtubule-motor proteins

Escalante-Ochoa

Ducatelle

Haesebrouck

2000

Microbial Pathogenesis

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Mode of Entry and Release of Chlamydiae in Infections of Intestinal Epithelial Cells

Cited by 42 publications

References 7 publications

The host adherens junction molecule nectin-1 is downregulated in Chlamydia trachomatis-infected genital epithelial cells

The host adherens junction molecule nectin-1 is downregulated in Chlamydia trachomatis-infected genital epithelial cells

Chlamydia trachomatis Cellular Exit Alters Interactions with Host Dendritic Cells

Optimal development of Chlamydophila psittaci in L929 fibroblast and BGM epithelial cells requires the participation of microfilaments and microtubule-motor proteins

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