Identification and Characterization of<i>Chlamydia pneumoniae</i>-Specific Proteins That Activate Tumor Necrosis Factor Alpha Production in RAW 264.7 Murine Macrophages

Jiang, Shangqing; Kuo, Cho‐Chou; Berry, Mark W.; Lee, Amy W.; Campbell, Lee Ann

doi:10.1128/iai.01331-07

Cited by 14 publications

(7 citation statements)

References 60 publications

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“…4B). The ability to activate EGR-1 has been reported with other pathogens, including group B Streptococcus and Chlamydia pneumoniae [42], [43]. NDRG1 is a cytoplasmic and nuclear protein involved in stress or hormone responses and cell growth and differentiation.…”

Section: Discussionmentioning

confidence: 95%

Coxiella burnetii, the Agent of Q Fever, Replicates within Trophoblasts and Induces a Unique Transcriptional Response

et al. 2010

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Q fever is a zoonosis caused by Coxiella burnetii, an obligate intracellular bacterium typically found in myeloid cells. The infection is a source of severe obstetrical complications in humans and cattle and can undergo chronic evolution in a minority of pregnant women. Because C. burnetii is found in the placentas of aborted fetuses, we investigated the possibility that it could infect trophoblasts. Here, we show that C. burnetii infected and replicated in BeWo trophoblasts within phagolysosomes. Using pangenomic microarrays, we found that C. burnetii induced a specific transcriptomic program. This program was associated with the modulation of inflammatory responses that were shared with inflammatory agonists, such as TNF, and more specific responses involving genes related to pregnancy development, including EGR-1 and NDGR1. In addition, C. burnetii stimulated gene networks organized around the IL-6 and IL-13 pathways, which both modulate STAT3. Taken together, these results revealed that trophoblasts represent a protective niche for C. burnetii. The activation program induced by C. burnetii in trophoblasts may allow bacterial replication but seems unable to interfere with the development of normal pregnancy. Such pathophysiologocal processes should require the activation of immune placental cells associated with trophoblasts.

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Section: Discussionmentioning

confidence: 95%

Coxiella burnetii, the Agent of Q Fever, Replicates within Trophoblasts and Induces a Unique Transcriptional Response

et al. 2010

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“…Fast mRNA synthesis of Egr1 has also been shown in several model systems of macrophage activation such as pathogen-mediated activation of RAW264.7 macrophages (Jiang et al 2008) and amyloid peptide stimulation of THP-1 cells (Giri et al 2005). This could indicate that different molecular mechanisms of myeloid cell activation could converge on the Egr1 signaling pathway.…”

Section: Discussionmentioning

confidence: 97%

Induction of Early Growth Response-1 Mediates Microglia Activation In Vitro But is Dispensable In Vivo

et al. 2009

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We have previously identified activation of microglia and induction of the early growth response gene 1 (Egr1) in the retina of retinoschisin-deficient (Rs1h(-/Y)) mice. We hypothesized that microglial expression of Egr1 might support retinal microgliosis. To test this, Egr1 transcript levels were determined in RNAs isolated from early postnatal retinas and primary microglia from Rs1h(-/Y) mice and wild-type controls. Egr1 mRNA expression was strongly induced in retinoschisin-deficient retinas as well as in ex vivo isolated microglia. Increased microglial Egr1 protein expression was concordantly detected in retinal sections of Rs1h(-/Y) mice using immunohistochemistry. Prominent activation-dependent Egr1 mRNA and protein expression was also confirmed in murine BV-2 microglia. Using binding site prediction and chromatin immunoprecipitation, we identified that the Egr1 promoter itself and the microglial marker genes Clec7a and Caspase11 are direct transcriptional targets of Egr1. Over-expression of Egr1 in BV-2 cells by adenoviral infection promoted Clec7a and Caspase11 mRNA synthesis, whereas expression of the Egr1 repressor NAB2 blocked the transcription of these genes. To analyze whether Egr1 was absolutely required for microglial marker expression in vivo, transcript levels were quantified in Rs1h(-/Y)/Egr1(-/-) retinas. No significant differences in activation marker expression could be measured in retinal tissue from Rs1h(-/Y)/Egr1(-/-) mice compared to Rs1h(-/Y) mice, suggesting that lack of Egr1 does not impair transcription of microglia genes in vivo. Taken together, our findings suggest that increased Egr1 expression is present in activated retinal microglia and contributes to their activation. However, up-regulation of Egr1 is not absolutely required for retinal microglia activation in vivo.

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“…CHSP10 recombinant plasmid was constructed with pQE30 vector (QIAGEN; Shanghai, China) and transformed into E. coli M15, induced, and purified as described elsewhere (Jiang et al 2008). Briefly, cells were cultured in Luria-Bertani broth containing 100 μg/mL ampicillin and 100 μg/mL kanamycin, harvested by centrifugation, and disrupted by sonication on ice; soluble His-tagged protein CHSP10 was purified by nickel-chelate affinity resin (QIAGEN) according to the manufacturer's protocol.…”

Section: Methodsmentioning

confidence: 99%

Heat shock protein 10 of Chlamydophila pneumoniae induces proinflammatory cytokines through Toll-like receptor (TLR) 2 and TLR4 in human monocytes THP-1

Zhou

Chen

et al. 2011

In Vitro Cell.Dev.Biol.-Animal

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Inflammatory response is the first line of infection. Previous studies have suggested that Chlamydophila pneumoniae heat shock protein (CHSP) 60 is present in human atheromata, and it plays an important role on the chronic infection elicited by C. pneumoniae. Here, we demonstrated in vitro the impact of heat shock protein 10 (HSP10) of C. pneumoniae on THP-1 cells and the role of Toll-like receptors (TLRs) in the procedures of inflammatory response. The production of proinflammatory cytokines, including tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-6, and IL-1beta were induced by recombinant HSP10 dose-dependently, and the proinflammatory activity of HSP10 was greatly reduced by heating and deproteinization treatment. The expression of TLR4 and TLR2 on the cultured cells were determined by reverse transcriptase-polymerase chain reaction and immunofluorescence. Peritoneal macrophages isolated from wild-type (C3H/HeN) and TLR4-deficient mice (C3H/HeJ) were respectively stimulated with endotoxin-free proteins. Cytokine responses after stimulation were significantly different, depending on the presence of TLR4. The effect on cytokine expression was blocked by anti-TLR2 or anti-TLR4 MAb partially or dramatically. Thus, HSP10 of C. pneumoniae which could elicit inflammatory reactions in human monocytes may contribute to the inflammatory processes in Chlamydophila infection, and the effects were mediated by TLR4 and, to a lesser extent, TLR2.

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Identification and Characterization ofChlamydia pneumoniae-Specific Proteins That Activate Tumor Necrosis Factor Alpha Production in RAW 264.7 Murine Macrophages

Cited by 14 publications

References 60 publications

Coxiella burnetii, the Agent of Q Fever, Replicates within Trophoblasts and Induces a Unique Transcriptional Response

Coxiella burnetii, the Agent of Q Fever, Replicates within Trophoblasts and Induces a Unique Transcriptional Response

Induction of Early Growth Response-1 Mediates Microglia Activation In Vitro But is Dispensable In Vivo

Heat shock protein 10 of Chlamydophila pneumoniae induces proinflammatory cytokines through Toll-like receptor (TLR) 2 and TLR4 in human monocytes THP-1

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