1,721,020 research outputs found

    Infectious burden and atherosclerosis. A clinical issue

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    Atherosclerotic cardiovascular diseases, chronic inflammatory diseases of multifactorial etiology, are the leading cause of death worldwide. In the last decade, more infectious agents, labeled as "infectious burden", rather than any single pathogen, have been showed to contribute to the development of atherosclerosis through different mechanisms. Some microorganisms, such as Chlamydia pneumoniae (C. pneumoniae), human cytomegalovirus, etc. may act directly on the arterial wall contributing to endothelial dysfunction, foam cell formation, smooth muscle cell proliferation, platelet aggregation as well as cytokine, reactive oxygen specie, growth factor, and cellular adhesion molecule production. Others, such as Helicobacter pylori (H. pylori), influenza virus, etc. may induce a systemic inflammation which in turn may damage the vascular wall (e.g., by cytokines and proteases). Moreover, another indirect mechanism by which some infectious agents (such as H. pylori, C. pneumoniae, periodontal pathogens, etc.) may play a role in the pathogenesis of atherosclerosis is molecular mimicry. Given the complexity of the mechanisms by which each microorganism may contribute to atherosclerosis, defining the interplay of more infectious agents is far more difficult because the pro-atherogenic effect of each pathogen might be amplified. Clearly, continued research and a greater awareness will be helpful to improve our knowledge on the complex interaction between the infectious burden and atherosclerosis

    New insights into Chlamydiae persistence: An energy metabolism strategy?

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    Chlamydiaceae is a family of obligate intracellular bacteria generally considered energy parasites. Several studies have suggested that Chlamydiae are capable of independently producing energy and, more importantly, several genes involved in the energy metabolism are up-regulated during the persistent state. Thus, it has been suggested that chlamydial persistence could be a complex and flexible metabolic strategy designed to favor a lengthy survival in the host cell by evading the immune response. In conclusion, more detailed studies on the shift in the chlamydial energy metabolism, from the active to the persistent form, may be helpful in future to determine whether chlamydial persistence observed in vitro does occur in vivo and whether chronic sequelae of chlamydial diseases may be related to the persistence. Copyright © by BIOLIFE, s.a.s.Chlamydiaceae is a family of obligate intracellular bacteria generally considered energy parasites. Several studies have suggested that Chlamydiae are capable of independently producing energy and, more importantly, several genes involved in the energy metabolism are up-regulated during the persistent state. Thus, it has been suggested that chlamydial persistence could be a complex and flexible metabolic strategy designed to favor a lengthy survival in the host cell by evading the immune response. In conclusion, more detailed studies on the shift in the chlamydial energy metabolism, from the active to the persistent form, may be helpful in future to determine whether chlamydial persistence observed in vitro does occur in vivo and whether chronic sequelae of chlamydial diseases may be related to the persistence

    Lyme borreliosis in Central Italy (1995-1998)

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    From January 1995 to July 1998, 340 serum samples collected in Central Italy from patients clinically suspected of having Lyme borreliosis were investigated. All samples were tested for the presence of antibodies to B. burgdorferi by Elisa. The Elisa positive samples were subjected to further tests by Western Blot for confirmation. Out of 340 patients, 13 (3.8%) proved to be B. burgdorferi positive, while 9 (2.6%) were found to have Lyme disease with seroprevalence being higher in these latter than that of blood donors from Central Italy. Our results indicate that Lyme borreliosis is present in Central Italy. A comparison between Italian and European studies reveals that Lyme disease is still underestimated in Italy, the main reason being that a monitoring system for the study of Lyme borreliosis was only established in 1990

    Updating the relationship of Chlamydia pneumoniae with atherosclerotic cardiovascular diseases. A systematic review of reviews

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    Chlamydia pneumoniae is the etiologic agent of respiratory tract infections in humans, including community-acquired pneumonia, and has been associated with atherosclerotic cardiovascular diseases. The present systematic review of reviews aimed at answering important questions on the involvement of C. pneumoniae in the pathogenesis of atherosclerosis, its cellular and molecular mechanisms, and whether there is evidence of a causal relationship. The databases PubMed/Med-line, Scopus, and Web of Science were searched for all review articles published from 2003 to the end of 2023. A total of 27 reviews, systematic reviews, and systematic reviews with metanalysis were included. Overall, current evidence suggests that C. pneumoniae is a biologically plausible candidate for the causation of atherosclerosis, albeit not all the 4 Koch postulates are fulfilled; oxidative stress and inflammation are the most likely pathogenic mechanisms mediated by C. pneumoniae. However, it is still unclear how the persistent form, responsible for chronic inflammation, fits into this etiopathogenetic scenario. In the future, the newly-designed transformation systems for the genomic manipulation of C. pneumoniae will surely help expand our knowledge on the role of this pathogen in atherogenesis

    Editorial for the Special Issue "Antibacterial activity of drug-resistant strains"

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    Antimicrobial resistance is an urgent global public health threat, as approximately 700,000 deaths annually can be attributed to antibiotic-resistant bacterial infections, and this figure is expected to reach 10 million deaths/year by 2050, a number that greatly exceeds the number of deaths resulting from cancer [...]

    Aspetti patogenetici delle infezioni da Chlamydiae

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    Negli ultimi anni le infezioni da Chlamydiae hanno destato un crescente interesse nella comunità scientifica, dal momento che oltre ad essere responsabili delle tradizionali patologie acute (infezioni genitali da parte di Chlamydia trachomatis; infezioni respiratorie da parte di C. pneumoniae e C. psittaci) sono state coinvolte in una serie di sequelae croniche di grande impatto sulla salute pubblica, tra le quali l'aterosclerosi. Lo scopo della nostra ricerca è stato quello di studiare gli aspetti patogenetici delle infezioni da Chlamydiae e a tal fine abbiamo allestito modelli in vitro di infezione con C. trachomatis e C. pneumoniae su linee cellulari epiteliali (HeLa ed HEp‐2) e linee macrofagiche J774A.1

    Chlamydia pneumoniae infection in atherosclerotic lesion development through oxidative stress: A brief overview

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    Chlamydia pneumoniae, an obligate intracellular pathogen, is known as a leading cause of respiratory tract infections and, in the last two decades, has been widely associated with atherosclerosis by seroepidemiological studies, and direct detection of the microorganism within atheroma. C. pneumoniae is presumed to play a role in atherosclerosis for its ability to disseminate via peripheral blood mononuclear cells, to replicate and persist within vascular cells, and for its pro-inflammatory and angiogenic effects. Once inside the vascular tissue, C. pneumoniae infection has been shown to induce the production of reactive oxygen species in all the cells involved in atherosclerotic process such as macrophages, platelets, endothelial cells, and vascular smooth muscle cells, leading to oxidative stress. The aim of this review is to summarize the data linking C. pneumoniae-induced oxidative stress to atherosclerotic lesion development

    The major epidemic infections: A gift from the old world to the new?

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    With the discovery of the New World, the Europeans flocked to America and with them spread infectious diseases. During long sea voyages the agents of these diseases increased their diffusion capacity in a suitable environment. Lack of hygiene, fatigue and privations, a diet without vitamins and many persons kept in confined spaces were the essential features of this enviroment. Sick persons, whose health conditions worsened during the journey to the New World, carried the germs of infectious diseases. The first disease to appear in the New World was smallpox described in 1518 in Hispaniola. From there the disease moved rapidly to Mexico in 1520, exterminating most of the Aztecs, Guatemala and to the territories of Incas from 1525-26, killing most of them and the King himself. The second disease, influenza, appeared in La Isabela, a few years later, causing a heavy epidemic between 1558 and 1559. Other diseases followed such as yellow fever and malaria. So Europeans and these invisible and mortal agents caused enormous destruction of American populations. In fact historians have estimated that beginning from early 1500, in only 50 years the population of Peru and Mexico fell from 60 to 10 million; in the latter country, in one century, the populations fell from an initial 10 million to only 2 million

    Growth kinetics of Chlamydia trachomatis in primary human Sertoli cells

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    Chlamydia trachomatis (Ct) is the leading cause of bacterial sexually transmitted infections worldwide and has been associated with male infertility. Recently, it was hypothesized that Ct may infect the epithelium of the seminiferous tubule, formed by Sertoli cells, thus leading to impaired spermatogenesis. To date, there is a lack of data on Ct infection of the seminiferous epithelium; therefore, we aimed to characterize, for the first time, an in vitro infection model of primary human Sertoli cells. We compared Ct inclusion size, morphology and growth kinetics with those in McCoy cells and we studied F-actin fibres, Vimentin-based intermediate filaments and α-tubulin microtubules in Sertoli and McCoy cells. Our main finding highlighted the ability of Ct to infect Sertoli cells, although with a unique growth profile and the inability to exit host cells. Furthermore, we observed alterations in the cytoskeletal fibres of infected Sertoli cells. Our results suggest that Ct struggles to generate a productive infection in Sertoli cells, limiting its dissemination in the host. Nevertheless, the adverse effect on the cytoskeleton supports the notion that Ct may compromise the blood-testis barrier, impairing spermatogenesis.</p
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