The pathogenesis of Pseudomonas aeruginosa disseminated infections depends on bacterial interaction with blood vessels. We have hypothesized that in order to traverse the endothelial barrier, bacteria would have to adhere to and damage endothelial cells. To test this hypothesis, we studied the adherence to human endothelial cells in primary culture of the piliated P. aeruginosa strain PAK and of two isogenic nonpiliated strains: PAK/p-, which carries a mutation in the pilin structural gene, and PAK-N1, a mutant defective in the regulatory rpoN gene. PAK adhered significantly more than did the pilus-lacking strains. P. aeruginosa was also taken up by endothelial cells, as determined by quantitative bacteriologic assays and by transmission electron microscopy. This internalization of P. aeruginosa seems to be a selective process, since the piliated strain was taken up significantly more than the nonpiliated bacteria and the avirulent Escherichia coli DH5 alpha, even following bacterial centrifugation onto the cell monolayers. A significant fraction of the internalized P. aeruginosa PAK was recovered in a viable form after 6 h of residence within endothelial cells. Progressive endothelial cell damage resulted from PAK intracellular harboring, as indicated by the release of lactate dehydrogenase. An increasing concentration of PAK cells was recovered from the extracellular medium with time, suggesting that ingested bacteria were released from endothelial cells and multiplied freely. We speculate that in vivo the ability of some P. aeruginosa strains to resist intracellular residence would afford protection from host defenses and antibiotics and that the release of viable bacteria into bloodstream may represent a central feature of the pathogenesis of bacteremia in compromised patients.
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http://dx.doi.org/10.1128/iai.62.12.5456-5463.1994 | DOI Listing |
J Assist Reprod Genet
January 2025
Ovarian Physiopathology Studies Laboratory, Institute of Experimental Biology and Medicine (IByME) - CONICET, Buenos Aires, Argentina.
Purpose: This study aimed to evaluate the long-term impact of mild COVID-19 infection and COVID-19 vaccination on ovarian function in patients undergoing assisted reproductive technology (ART). Specifically, we assessed ovarian outcomes between 9 and 18 months post-infection and investigated the effects of COVID-19 vaccines (inactivated virus and adenovirus) on reproductive parameters.
Methods: The study included two objectives: (a) examining ovarian function in post-COVID-19 patients (9-18 months post-infection) compared to a control group and (b) comparing reproductive outcomes in vaccinated versus unvaccinated patients.
Biomarkers
January 2025
PMI R&D, Philip Morris Products S.A., Neuchâtel, Switzerland.
Background: Growing evidence indicates that noncombustible products could be a tobacco harm reduction tool for smokers who do not quit. The Tobacco Heating System (THS) emits substantially lower levels of harmful cigarette smoke constituents, and previous randomized clinical studies showed improved levels of biomarkers of potential harm (BoPH) linked to smoking-related disease.
Methods: In this cross-sectional study of healthy participants (n = 982) who (i) smoked cigarettes, (ii) had voluntarily switched from smoking to THS use, or (iii) formerly smoked, blood and urine samples were assayed for nine BoPH.
Arterioscler Thromb Vasc Biol
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Research Center of Clinical Medicine, Affiliated Hospital, Nantong University, China. (X.W., D.L.).
Background: Hyperglycemia is a major contributor to endothelial dysfunction and blood vessel damage, leading to severe diabetic microvascular complications. Despite the growing body of research on the underlying mechanisms of endothelial cell (EC) dysfunction, the available drugs based on current knowledge fall short of effectively alleviating these complications. Therefore, our endeavor to explore novel insights into the cellular and molecular mechanisms of endothelial dysfunction is crucial for the field.
View Article and Find Full Text PDFArterioscler Thromb Vasc Biol
January 2025
Department of Cardiovascular Medicine, The University of Tokyo, Bunkyo-ku, Japan. (H. Yagi, H.A., Q.L., A.S.-K., M.U., H.K., R.M., A.S., S.O., H.T., Norifumi Takeda, I.K.).
Background: Marfan syndrome (MFS) is an inherited disorder caused by mutations in the gene encoding fibrillin-1, a matrix component of extracellular microfibrils. The main cause of morbidity and mortality in MFS is thoracic aortic aneurysm and dissection, but the underlying mechanisms remain undetermined.
Methods: To elucidate the role of endothelial XOR (xanthine oxidoreductase)-derived reactive oxygen species in aortic aneurysm progression, we inhibited in vivo function of XOR either by endothelial cell (EC)-specific disruption of the gene or by systemic administration of an XOR inhibitor febuxostat in MFS mice harboring the missense mutation p.
J Tissue Eng
January 2025
Department of Surgery, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Mural cells are essential for maintaining the proper functions of microvasculatures. However, a key challenge of microvascular tissue engineering is identifying a cellular source for mural cells. We showed that , circulating fibrocytes (CFs) can (1) shear and stabilize the microvasculatures formed by vascular endothelial cells (VECs) in a collagen gel, (2) form gap junctions with VECs and (3) induce basement membrane formation.
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