Publications by authors named "Lee Ann Campbell"
Article Synopsis
- In 2020, the International Committee on Systematics of Prokaryotes (ICSP) rejected a proposal to change the naming rules for prokaryotes to include gene sequences as a basis for nomenclature.
- In 2022, an alternative naming system called SeqCode was introduced, allowing genome sequences to be used for naming species.
- The ICSP's taxonomy subcommittee believes that using gene sequences could improve naming for hard-to-culture microorganisms, like chlamydiae, and suggests registering new names for uncultured prokaryotes in the SeqCode registry.
Article Synopsis
- * Many rectal infections are asymptomatic, leading to uncertainties about their health impacts, particularly for women, and there are significant gaps in understanding how these infections spread and their overall clinical importance.
- * Recent studies suggest gastrointestinal infections might influence immune responses related to urogenital infections, raising questions about their implications for developing a CT vaccine and highlighting the need for more research in this area.
Article Synopsis
- The study aimed to evaluate the prevalence of Chlamydia pneumoniae in children with respiratory infections by analyzing samples from 416 children in Sao Luis, Brazil.* -
- Among the participants, kids with upper respiratory tract infections showed a 38.2% positivity rate for C. pneumoniae, while those with community-acquired pneumonia had an 18.0%, compared to just 7.9% in asymptomatic controls.* -
- Overall, the findings indicate a significant association of C. pneumoniae with respiratory infections, highlighting particularly higher DNA levels in children with upper respiratory tract infections.*
Article Synopsis
- The study examines the anti-inflammatory effects of the ethyl acetate fraction from pomegranate leaves (EAFPg) on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in a mouse model.
- Male Swiss mice were treated with varying doses of EAFPg or dexamethasone before LPS exposure, and results showed that EAFPg significantly reduced neutrophil accumulation and collagen deposition in the lungs.
- Additionally, EAFPg and kaempferol decreased nitric oxide production and cytokine expression in cultured macrophages, indicating potential therapeutic value for EAFPg in treating lung inflammation.
Article Synopsis
- Chlamydia pneumoniae (Cpn) is linked to cardiovascular disease and can worsen atherosclerosis, while murine norovirus (MNV) affects atherosclerosis differently in mouse models.
- Researchers studied the impact of Cpn and MNV coinfection on macrophage behavior and atherosclerosis in mice lacking certain cholesterol receptors, finding that coinfection increased inflammatory gene expression in lab cultures.
- Despite the inflammatory response observed in vitro, MNV did not significantly change plaque sizes in vivo when coinfected with Cpn in mice, indicating that MNV doesn’t have a major effect on Cpn-driven plaque development.
Article Synopsis
- * While the buildup of lipids is a main driver of atherosclerosis, evidence suggests that infections may also play a significant role in the disease process.
- * The review will explore specific infectious agents linked to atherosclerosis and discuss the difficulties in proving their involvement in human cases, despite supporting animal model studies.
Article Synopsis
- * Direct infection of bovine aortic smooth muscle cells didn't lead to calcification, but factors from infected macrophages stimulated these cells to adopt a calcifying phenotype.
- * The findings suggest that substances released during C. pneumoniae infection can increase inflammation and promote collagen production, which may contribute to the calcification and fibrosis seen in atherosclerosis.
Persistent C. pneumoniae infection in atherosclerotic lesions: rethinking the clinical trials.
Front Cell Infect Microbiol
September 2014
Article Synopsis
- 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.
Article Synopsis
- 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.
Article Synopsis
- 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.
Article Synopsis
- The study aimed to evaluate the effectiveness of rifalazil, an antibiotic targeting Chlamydia pneumoniae, in improving peak walking time for patients with symptomatic peripheral artery disease.
- A total of 297 patients were randomly assigned to receive either rifalazil or a placebo, with assessments made 180 days after starting treatment.
- The results indicated that rifalazil did not significantly enhance peak walking time or quality of life compared to placebo, with both groups showing similar improvements.
Article Synopsis
- 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.
Efficacy of benzoxazinorifamycins in a mouse model of Chlamydia pneumoniae lung infection.
Antimicrob Agents Chemother
May 2008
Article Synopsis
- 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.
Article Synopsis
- 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
Article Synopsis
- 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.
Article Synopsis
- 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.
Article Synopsis
- 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.
Development potential of rifalazil and other benzoxazinorifamycins.
Expert Opin Investig Drugs
June 2006
Article Synopsis
- Rifalazil and other benzoxazinorifamycins are new antibacterial drugs effective against intracellular pathogens like Chlamydia, showing promise in treating sexually transmitted diseases.
- These compounds, particularly rifalazil, have strong tissue penetration and high activity against related bacteria, including C. pneumoniae, and are being studied for various conditions such as peripheral arterial disease and gastric ulcers.
- Unlike traditional rifampin, rifalazil and its counterparts do not disrupt cytochrome P450 3A4, reducing the risk of harmful drug interactions.
Article Synopsis
- 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.
Article Synopsis
- 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
Article Synopsis
- 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.
Article Synopsis
- * 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).
Article Synopsis
- 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.