Publications by authors named "Cho-Chou Kuo"

The family Chlamydiaceae (order Chlamydiales, phylum Chlamydiae) comprises important, obligate intracellular bacterial pathogens of humans and animals. Subdivision of the family into the two genera Chlamydia and Chlamydophila has been discussed controversially during the past decade. Here, we have revisited the current classification in the light of recent genomic data and in the context of the unique biological properties of these microorganisms.

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Several lines of evidence have associated Chlamydia pneumoniae with cardiovascular disease including acceleration of atherosclerotic lesion progression in hyperlipidemic animal models by infection. Many of the pro-atherogenic effects of oxidized low-density lipoprotein (ox-LDL) occur through the activation of the lectin-like ox-LDL receptor-1 (LOX-1). Chlamydia pneumoniae upregulates the expression of the LOX-1 mRNA, promotes the uptake of ox-LDL, and utilizes the LOX-1 receptor for infectivity.

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  • Chlamydia pneumoniae is linked to atherosclerosis and increases the expression of LOX-1 in endothelial cells, which plays a role in atherosclerosis progression.
  • The study found that infection by C. pneumoniae is specifically inhibited by LOX-1 ligands and antibodies, while other scavenger receptors do not show this effect.
  • Evidence demonstrates that C. pneumoniae binds to the LOX-1 receptor and co-localizes with it, highlighting its role in promoting atherosclerosis, unlike other Chlamydia species.
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  • Researchers studied the immune response in mice infected with Chlamydia pneumoniae over 72 hours, finding increased levels of certain inflammatory markers like IL-2, IL-5, and IFN-gamma, but no rise in TNF-alpha or IL-1beta.
  • The infection led to decreased activity of a protective enzyme (paraoxonase) and reduced ability of HDL to prevent cellular oxidation, indicating a potential link between the infection and heart health.
  • In older mice, infection with live C. pneumoniae resulted in more frequent intra-plaque hemorrhages in arteries, implying that the immune response may worsen plaque stability and contribute to atherosclerosis progression.
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  • Chlamydia pneumoniae is a Gram-negative bacterium that causes various respiratory diseases and is linked to cardiovascular issues.
  • It requires specific cell lines (like HL and HEp-2) for growth and isolation, making it harder to culture compared to Chlamydia trachomatis.
  • Successful isolation involves centrifuging the sample onto cell layers, using cycloheximide, and staining with specific antibodies, while careful handling during culture is crucial.
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  • Chlamydia pneumoniae is linked to cardiovascular disease and worsens atherosclerosis in animals with high cholesterol.
  • Retinoic acid acts as an antioxidant that inhibits C. pneumoniae infections in these endothelial cells, reducing disease progression.
  • In a study with hyperlipidemic mice, retinoic acid treatment lowered the severity of foam cell lesions caused by C. pneumoniae without affecting uninfected mice, likely by reducing lung infection duration.
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  • Researchers tested rifalazil and other benzoxazinorifamycins for treating lung infections caused by Chlamydia pneumoniae in mice.
  • The treatment consisted of administering one dose per day for three days at dosages of either 3 or 1 mg/kg of body weight.
  • All tested compounds, including rifalazil, demonstrated effectiveness in combating the infection.
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  • Chlamydia pneumoniae, a common respiratory pathogen, activates macrophages, leading to inflammatory responses that may contribute to atherosclerosis, although the specific antigens responsible were not well understood.
  • The study focused on three chlamydial proteins (OMP2, Cpn 0980, and Cpn 0809) and demonstrated that they can activate macrophages by inducing the expression of TNF-alpha and tissue factor, as well as activating certain signaling pathways (p44/42 MAPK and Egr-1).
  • The research also indicated that the activation of macrophages by these proteins involves Toll-like receptors (TLR2 and TLR4), as their absence significantly reduced the inflammatory response, thus highlighting a potential
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  • Chlamydia pneumoniae is a respiratory pathogen linked to cardiovascular disease, promoting atherosclerosis and LDL oxidation.
  • All-trans-retinoic acid (ATRA), an antioxidant, inhibits C. pneumoniae infection by blocking its attachment to endothelial cells via the M6P/IGF2 receptor.
  • This study explores ATRA's effects on epithelial cells, revealing it disrupts C. pneumoniae attachment through the M6P/IGF2 receptor and inhibits cell growth via nuclear receptors.
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  • The study investigates how Chlamydia pneumoniae infection influences the adherence of macrophages to endothelial cells, an early step in atherosclerosis development.
  • GFP-transgenic mice were used to show that C. pneumoniae-infected macrophages exhibited increased adherence to both endothelial cells in lab settings and to aortas from normal and high cholesterol mice in ex vivo tests.
  • The research highlights that ICAM-1 is essential for this enhanced adherence, indicating its role in the process by which C. pneumoniae accelerates the progression of atherosclerosis.
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  • Previous research indicates that the chlamydial glycan, featuring a high-mannose oligosaccharide, is essential for the organism's attachment and infectivity.
  • Removing this glycan leads to a significant decrease in the organism's ability to infect both in laboratory settings (in vitro) and in live animals (in vivo).
  • The current study reveals that administering chlamydial organisms alongside a ligand that blocks glycan binding can reduce the amount of chlamydia in the lungs of infected animals.
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  • Previous research identified a specific high-mannose oligosaccharide in Chlamydia that plays a key role in its ability to attach and infect host cells.
  • Removing this glycan from the organism was shown to lower its infectivity in lab settings.
  • The current study further reveals that using N-glycanase on Chlamydia significantly reduces or completely eliminates its infectivity in living organisms.
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Infections caused by the obligate intracellular pathogen Chlamydia trachomatis have a marked impact on human health. C. trachomatis serovariants are the leading cause of bacterial sexually transmitted disease and infectious preventable blindness.

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  • Multiple mechanisms for how Chlamydia attaches and enters cells have been studied, revealing that Chlamydia trachomatis's major outer membrane protein can affect its infectivity in epithelial cells.
  • A hapten inhibition assay was conducted to test the role of the mannose 6-phosphate (M6P)/IGF2 receptor in Chlamydia pneumoniae's infection of endothelial cells, with findings indicating that M6P and related compounds can inhibit this process.
  • Results showed that while C. pneumoniae can use the M6P/IGF2 receptor for attachment and entry into cells, C. trachomatis does not rely on this mechanism, highlighting a key difference in how these two Chlamydia species
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  • Chlamydiae are dependent on host cells for energy (ATP) and their infection can disrupt the normal ATP levels, leading to increased cell death.
  • Research showed that both live and inactivated C. pneumoniae can increase ATP levels in mouse macrophages, but the effects differ based on the condition of the bacteria (live vs. inactivated) and the infection dosage (MOI).
  • The ability of C. pneumoniae to boost ATP content in macrophages relies on the presence of specific Toll-like receptors (specifically TLR2 and MyD88), while it does not affect cells lacking TLR4.
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  • * Research shows that C. pneumoniae infection can increase cell death in macrophages exposed to oxidized LDL, indicating it worsens cardiovascular risk without causing typical apoptosis markers.
  • * The study suggests that C. pneumoniae may kill macrophages through a caspase-independent pathway, potentially involving the activation of Toll-like receptor 2 (TLR-2).
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  • The study examined how tumor necrosis factor alpha (TNF-alpha) impacts the development of atherosclerosis in mice infected with Chlamydia pneumoniae.
  • Researchers used a specific breed of mice that lacked the TNF-alpha p55 receptor and fed them a high-fat/high-cholesterol diet.
  • Findings showed no difference in atherosclerotic lesion development between infected and uninfected mice, suggesting that TNF-alpha contributes to accelerating atherosclerosis caused by C. pneumoniae.
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Previous studies demonstrated that the high-mannose oligosaccharide N linked to the Chlamydia major outer membrane protein inhibited the attachment and infectivity of the organism. The present study showed that cleavage of the glycan with N-glycanase decreased the attachment and infectivity of chlamydial organisms in human epithelial and endothelial cells.

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Background: Inflammatory processes are an integral component of the initiation, progression, and destabilization of atherosclerotic lesions. Tumor necrosis factor-alpha (TNF-alpha) is considered a primary mediator of inflammatory processes.

Methods And Results: The role of TNF-alpha in plaque progression and plaque destabilization was investigated in the innominate arteries of older TNF-alpha receptor p55 deficient mice that were generated on a hyperlipidemic apolipoprotein E deficient background (p55-/- apoE-/-).

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Macrophages play a critical role in both innate and acquired immunity because of their unique ability to internalize, kill, and degrade bacterial pathogens through the process of phagocytosis. The adaptor protein, amphiphysin IIm, participates in phagocytosis and is transiently associated with early phagosomes. Certain pathogens, including Chlamydia pneumoniae, have evolved mechanisms to subvert macrophage phagosome maturation and, thus, are able to survive within these cells.

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Chlamydial delayed-type hypersensitivity antigens were analyzed by using the subcutaneous salpingeal autotransplant model of Macaca nemestrina infected with Chlamydia trachomatis serovar E. Heat shock protein 60 was the only antigen shown to induce delayed-type hypersensitivity among other antigens tested, including UV-inactivated organisms, recombinant major outer membrane protein, purified outer membrane proteins, and heat shock protein 10.

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Objective: Inflammation contributes to atherosclerotic plaque initiation and progression. Recent studies suggest that anti-inflammatory drugs such as cyclooxygenase-2 (Cox-2) inhibitors have anti-atherogenic effects. The current study was designed to investigate whether administration of a Cox-2 inhibitor to older apolipoprotein E deficient (apo E-/-) mice with established lesions alters the composition and increases the stability of the lesions.

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Objective: Chlamydia pneumoniae infection has been associated with atherosclerosis, although the mechanisms by which C. pneumoniae contribute to atherogenesis remain unclear. Altered production of nitric oxide, a known bactericidal and anti-inflammatory agent, represents one possible mechanistic link.

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Chlamydia pneumoniae is a human respiratory pathogen that causes acute respiratory disease. Multiple studies have associated C. pneumoniae with cardiovascular disease including seroepidemiologic studies, direct detection of the organism within the lesion, and isolation of the organism from atheromatous tissue.

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