Nuclear Factor–κB Activation in Endothelium by<i>Chlamydia pneumoniae</i>without Active Infection

Baer, Jefferson; Laney, Tracey V. du; Wyrick, Priscilla B.; McCain, Arlene S.; Fischer, Thomas; Merricks, Elizabeth P.; Baldwin, Albert S.; Nichols, Timothy C.

doi:10.1086/378564

Cited by 20 publications

(12 citation statements)

References 15 publications

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“…Previously, heat or formalin inactivated C. pneumoniae were shown to induce NFκB nuclear translocation in porcine endothelial cells (Baer et al, 2003), while heat inactivated C. pneumoniae was incapable of activating an NFκB luciferase reporter assay in human vascular endothelial cells (Opitz et al, 2005). This suggests that the host cells, and potentially the method of NFκB activation assay, may play a role in the requirement for chlamydial viability in NFκB activation.…”

Section: Discussionmentioning

confidence: 99%

Productive and Penicillin-Stressed Chlamydia pecorum Infection Induces Nuclear Factor Kappa B Activation and Interleukin-6 Secretion In Vitro

Leonard

Schoborg

Borel

2017

Front. Cell. Infect. Microbiol.

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Nuclear factor kappa B (NFκB) is an inflammatory transcription factor that plays an important role in the host immune response to infection. The potential for chlamydiae to activate NFκB has been an area of interest, however most work has focused on chlamydiae impacting human health. Given that inflammation characteristic of chlamydial infection may be associated with severe disease outcomes or contribute to poor overall fitness in farmed animals, we evaluated the ability of porcine chlamydiae to induce NFκB activation in vitro. C. pecorum infection induced both NFκB nuclear translocation and activation at 2 hours post infection (hpi), an effect strongly enhanced by suppression of host de novo protein synthesis. C. suis and C. trachomatis showed less capacity for NFκB activation compared to C. pecorum, suggesting a species-specific variation in NFκB activation. At 24 hpi, C. pecorum induced significant NFκB activation, an effect not abolished by penicillin (beta lactam)-induced chlamydial stress. C. pecorum-dependent secretion of interleukin 6 was also detected in the culture supernatant of infected cells at 24 hpi, and this effect, too, was unchanged by penicillin-induced chlamydial stress. Taken together, these results suggest that NFκB participates in the early inflammatory response to C. pecorum and that stressed chlamydiae can promote inflammation.

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Section: Discussionmentioning

confidence: 99%

Productive and Penicillin-Stressed Chlamydia pecorum Infection Induces Nuclear Factor Kappa B Activation and Interleukin-6 Secretion In Vitro

Leonard

Schoborg

Borel

2017

Front. Cell. Infect. Microbiol.

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“…Infection of cells with the related species Chlamydia pneumoniae results in NF-B activation (28), but it is unclear what role this plays in the prevention of host cell death. Specifically, NF-B activation occurs upon inoculation with nonviable C. pneumoniae (1), but the inhibition of apoptosis requires live replicating bacteria (25), thus indicating that activation of the NF-B pathway alone is not sufficient to protect cells from apoptosis. In a similar fashion, the NF-B pathway may not be a central effector for inhibiting apoptosis during N. caninum infection.…”

Section: Discussionmentioning

confidence: 99%

The Apicomplexan PathogenNeospora caninumInhibits Host Cell Apoptosis in the Absence of Discernible NF-κB Activation

Herman¹,

Molestina

Sinai

et al. 2007

Infect Immun

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Neospora caninum, a causative agent of bovine abortions, is an apicomplexan parasite that is closely related to the human pathogen Toxoplasma gondii. Since a number of intracellular parasites, including T. gondii, have been shown to modulate host cell apoptosis, the present study was conducted to establish whether N. caninum is similarly capable of subverting apoptotic pathways in its host cells. Our results indicated that death receptor-mediated apoptosis is repressed during N. caninum infection, and the data further showed that the executioner caspase, caspase 3, does not become activated in the infected cells. Surprisingly, nuclear translocation of the NF-B subunit p65 was not detected in N. caninum-infected cells, although this host transcription factor has been shown to upregulate prosurvival genes in cells infected with T. gondii. Consistent with these findings, the distinct accumulation of phosphorylated IB that is seen at the parasitophorous vacuole membrane (PVM) of T. gondii was not apparent on the N. caninum PVM. Although a putative IB kinase activity was detected in N. caninum extracts, thereby implying that this parasite is capable of modulating NF-B translocation into the host cell nucleus, the data collectively suggest that a profound and sustained activation of the NF-B pathway is not central to the ability of N. caninum to prevent apoptosis of their host cells.

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“…Our data on the NF‐κB‐induced upregulation of cIAP‐2 protein and the requirement of cIAP‐1 and cIAP‐2 for maintaining the apoptosis resistance, however, suggest an additional level of regulation. The finding that NF‐κB is required for apoptosis resistance is particularly interesting because acute C. pneumoniae has been shown to induce the translocation of NF‐κB in a variety of cell lines, for example, in monocytes (Wahl et al ., 2001; 2003; Donath et al ., 2002), in epithelial cell lines HL and Calu3 (Gencay et al ., 2003), in human smooth muscle cells (Dechend et al ., 1999; Miller et al ., 2000) and in endothelial cells (Dechend et al ., 1999; Krull et al ., 1999; Molestina et al ., 2000; Baer et al ., 2003). Thus, an involvement of NF‐κB in Cpn infection‐induced apoptosis resistance of other cell types is very likely.…”

Section: Discussionmentioning

confidence: 99%

NF-?B and inhibitor of apoptosis proteins are required for apoptosis resistance of epithelial cells persistently infected with Chlamydophila pneumoniae

et al. 2006

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Nuclear Factor–κB Activation in Endothelium byChlamydia pneumoniaewithout Active Infection

Cited by 20 publications

References 15 publications

Productive and Penicillin-Stressed Chlamydia pecorum Infection Induces Nuclear Factor Kappa B Activation and Interleukin-6 Secretion In Vitro

Productive and Penicillin-Stressed Chlamydia pecorum Infection Induces Nuclear Factor Kappa B Activation and Interleukin-6 Secretion In Vitro

The Apicomplexan PathogenNeospora caninumInhibits Host Cell Apoptosis in the Absence of Discernible NF-κB Activation

NF-?B and inhibitor of apoptosis proteins are required for apoptosis resistance of epithelial cells persistently infected with Chlamydophila pneumoniae

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