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Alternations of lipid metabolism can be induced by pharmacological agents (as azithromycin, a macrolide antibiotic) or by nutriments (as glucose). These alterations can promote some pathology like atherosclerosis.
In THP-1, a human leukemia monocytic cell line, either undifferentiated or differentiated by PMA, we tested the effect of azithromycin and glucose on the accumulation of phospholipids and cholesterol, as well as the influence of oxidized LDL on these accumulations.
We showed that azithromycin, at the concentration of 50 μg/ml, induces an accumulation of phospholipids and cholesterol is undifferentiated and differentiated macrophages THP-1. In THP-1 non differentiated cells, the accumulation of cholesterol was due to an elevation of free cholesterol, whereas in cells differentiated by PMA, cholesterol was accumulated in its ester form. When the cells were incubated with glucose, no accumulation of lipids was evidenced.
When cells differentiated by PMA were incubated with oxidized LDL, we showed that azithromycin, at the concentration of 50 μg/ml or higher, induced cholesterol accumulation. In contrast, when cells were incubated in the presence of increasing concentrations of glucose, no cholesterol accumulation was found. Neither azithromycin nor glucose, were able to modulate the expression of the scavenger receptor CD36 (one of the receptors to oxidized LDL).
Our study has shown that azithromycin is bale to induce a lipid accumulation in THP-1 cell-line. The antibiotic can stimulate the accumulation of cholesterol when the cells are incubated with oxidized LDL. This may suggest a possible effect of azithromycin on artherogenesis. Even though a possible link has been proposed between hyperglycemia and cardiovascular disease, we do not show any effect of glucose on the accumulation of lipids Les désordres du métabolisme lipidique par des agents pharmacologiques (tel que l’azithromycine, un antibiotique de la classe des macrolides) ou par des nutriments (comme le glucose) et être à l’origine de pathologies dont l’athérosclérose.
Dans un modèle de monocytes humains, les THP-1, non différenciés ou différenciés à l’aide de PMA, nous avons étudié l’effet de l’azithromycine et du glucose sur l’accumulation de phospholipides et de cholestérol ainsi que l’influence sur ces paramètres de LDL oxydées dans le milieu de culture.
Nous avons montré que l’azithromycine, à une concentration de 50 μg/ml, induit à la fois une surcharge en phospholipides et en cholestérol au sein des THP-1 qu’ils soient différenciés ou non en macrophages. A l’état monocytaire, la surcharge en cholestérol est liée à une révélation du contenu cellulaire en cholestérol libre tandis que les cellules différenciées en macrophages présentent une surcharge en cholestérol estérifié.
En présence de glucose, nous n’avons pas observé de surcharges lipidiques au sein des THP-1.
Lorsque les LDL oxydées sont rajoutées au milieu de culture des THP-1 différenciés en macrophages, l’azithromycine , à une concentration égale ou supérieure à 50 μg/ml, induit une accumulation de cholestérol. Par contre, des concentrations croissantes en glucose ne modifient pas l’accumulation de cholestérol liée à la capture des LDL oxydées. Que ce soit en présence de l’agent pharmacologique ou nutritionnel, nous n’avons pas observé de modifications dans l’expression du scavenger receptor CD36, l’un des récepteurs assurant l’internalisation des LDL oxydées.
D’après notre étude, l’azithromycine est capable d’induire des surcharges lipidiques au sein d’une lignée cellulaire humaine et peut, à partir d’une certaine concentration, favoriser la capture de LDL oxydées. Ces données suggèrent un effet possible de l’azithromycine sur le processus de l’athérogénèse. Malgré qu’il puisse y avoir un lien entre une hyperglycémie et la survenue de troubles cardio-vasculaires, nous n’avons pas montré d’effet du glucose que ce soit sur les surcharges lipidiques ou sur la capture de LDL oxydées

Azithromycin --- Glucose --- Cholesterol, LDL --- Phospholipids --- Sphingolipids

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Background : Airway inflammation is of pivotal importance in cystic fibrosis (DF) lung disease. We have previously demonstrated in F508del-CF mice a lung inflammation characterized by macrophage infiltration which reduced after azithromycin treatment. The present study aimed at characterizing phenotype of macrophages isolated from wild-type or F508del-CF (CF) mice and assessing the effects of azithromycin on these immune cells.
Methods : Macrophages purified from lung and peritoneal cavity were stimulated either with lipopolysaccarides from Pseudomonas aeruginosa plus interferon-γ or with interleukin-(IL)-4 plus IL-13, either in the presence or in the absence of 1mg/l azithromycin. Macrophage phenotypes were investigated in primary culture 6h after stimulation by different M1 (pro-inflammatory) and M2 (anti-inflammatory) markers at the mRNA level.
Results : A marked macrophage infiltration was observed in both lungs and peritoneal cavity suggesting a systemic macrophage accumulation in CF mice. Non-stimulated and stimulated CF peritoneal macrophages overexpressed M1 (IL1-β and TNF-α) and M2 (Arginase-1, IL-10 and A20) markers as compared to wild-type peritoneal cells. Similar pattern of responses to M1 and M2 stimuli were observed in CF alveolar macrophages. These findings indicated that the immune responses are exacerbated in CF macrophages. Curiously, in non-stimulated CD alveolar macrophages the expression of M1 and M2 mediators was down-regulated. Moreover, we found that azithromycin reduced M1 macrophages activation in CF and wild-type alveolar macrophage.
Conclusions : Our findings further support the concept that overall macrophage immune responses are altered in CF and that azithromycin particularly downregulates M1 differentiation

Cystic Fibrosis --- Phenotype --- Azithromycin --- Macrophages --- Mice --- Cystic Fibrosis Transmembrane Conductance Regulator

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This book is a compilation of articles by experts on the prevention and treatment of periodontal disease, many of which are full of data-based evidence from basic research perspectives or patient data.

Medicine --- 70-kDa heat shock proteins --- gingival crevicular fluid --- heat shock protein --- periodontitis --- periodontal disease --- diabetes --- diabetic retinopathy --- bleeding on probing --- probing pocket depth --- fasting blood sugar --- carotid artery calcification --- alveolar bone loss --- computed tomography --- panoramic radiographs --- aspiration pneumonia --- chronic periodontitis --- Porphyromonas gingivalis --- proinflammatory cytokines --- TLR2 --- epidemiological index --- item response theory --- oral examination --- diagnosis --- Mfa1 --- Toll-like receptors --- gingival fibroblast --- azithromycin --- human gingival fibroblast --- human periodontal ligament fibroblast --- IL-6 --- IL-8 --- MMP-1 --- MMP-2 --- chewing ability --- infection --- inflammation --- periodontal medicine --- Gan-Lu-Yin --- herbal medicine --- osteoclastogenesis --- periodontal diseases --- periodontal pocket --- health status indicators --- periodontal inflamed surface area (PISA) --- rheumatoid arthritis --- tocilizumab --- periodontal inflamed surface area --- periodontal pathogen --- mixed effect modeling --- follow-up study --- Low reactive Level Laser Therapy (LLLT) --- human gingival fibroblasts (HGF) --- microarray --- differentially gene expression (DEGs) --- gene ontology --- biological processes (BP) --- protein–protein interaction (PPI)

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"COVID-19 has killed more people than any war or public health crisis in American history, but the scale and grim human toll of the pandemic were not inevitable. Pandemic Politics examines how Donald Trump politicized COVID-19, shedding new light on how his administration tied the pandemic to the president's political fate in an election year and chose partisanship over public health, with disastrous consequences for all of us. Health is not an inherently polarizing issue, but the Trump administration's partisan response to COVID-19 led ordinary citizens to prioritize what was good for their "team" rather than what was good for their country. Democrats seized on the crisis as evidence of Trump's indifference to public well-being. At a time when solidarity and bipartisan unity was sorely needed, Americans came to see the pandemic in partisan terms, adopting behaviors and attitudes that continue to divide us today. This book draws on a wealth of new data on public opinion to show how pandemic politics has touched all aspects of our lives-from the economy to race and immigration-and puts America's COVID-19 response in global perspective. An in-depth account of a uniquely American tragedy, Pandemic Politics reveals how the politicization of the COVID-19 pandemic has profound and troubling implications for public health and the future of democracy itself"--

COVID-19 Pandemic, 2020 --- -Political aspects --- Trump, Donald, --- United States --- Politics and government --- Accountability. --- Aid. --- Alaska Natives. --- Alex Azar. --- Allergy. --- Aluminium foil. --- Asian Americans. --- Asymmetry. --- Audrey Tang. --- Authority. --- Azithromycin. --- Border control. --- Boris Johnson. --- Breitbart News. --- Business loan. --- Career. --- Chapter 9. --- Chloroquine. --- Citizenship of the United States. --- Civil society. --- Coronavirus. --- Covid-19. --- Credibility. --- Democracy. --- Developed country. --- Disease. --- Disgust. --- Distrust. --- Economic indicator. --- Economic recovery. --- Emergency Fund. --- Employment. --- Ethnic group. --- Expenditure. --- Finding. --- Frustration. --- Guideline. --- Hate crime. --- Health care. --- Health system. --- Hospital bed. --- Immigration. --- Incidence (epidemiology). --- Income. --- Investment. --- Joe Biden. --- La Jolla. --- Law. --- Liberty. --- MSNBC. --- Medicine. --- Mobile phone. --- Morale. --- Mutual aid (organization theory). --- Narrative. --- Northern Italy. --- Nursing. --- Of Education. --- Open border. --- Opposition Party. --- Pejorative. --- Percentage point. --- Pfizer. --- Phases of clinical research. --- Phil Valentine. --- Policy. --- Political positions of Donald Trump. --- Politician. --- Politics of the United States. --- Politics. --- Presidential nominee. --- Preventable causes of death. --- Recession. --- Recommendation (European Union). --- Representative democracy. --- Respondent. --- Sadness. --- Salary. --- Science. --- Scientist. --- Seriousness. --- Severity (video game). --- Sewing machine. --- Sinopharm. --- Small business. --- Smallpox. --- Social determinants of health. --- State government. --- Steve Inskeep. --- Strategic partnership. --- Supporter. --- Tax credit. --- Tax cut. --- Uncertainty. --- Unemployment. --- Vaccination. --- Vaccine. --- Wavenumber. --- Weapon. --- World Health.