BackgroundThroughout Europe, Ixodes ricinus transmits numerous pathogens. Its widespread distribution is not limited to rural but also includes urbanized areas. To date, comprehensive data on pathogen carrier rates of I. ricinus ticks in urban areas of Switzerland is lacking.Results Ixodes ricinus ticks sampled at 18 (sub-) urban collection sites throughout Switzerland showed carrier rates of 0% for tick-borne encephalitis virus, 18.0% for Borrelia burgdorferi (sensu lato), 2.5% for Borrelia miyamotoi, 13.5% for Rickettsia spp., 1.4% for Anaplasma phagocytophilum, 6.2% for "Candidatus Neoehrlichia mikurensis", and 0.8% for Babesia venatorum (Babesia sp., EU1). Site-specific prevalence at collection sites with n > 45 ticks (n = 9) significantly differed for B. burgdorferi (s.l.), Rickettsia spp., and "Ca. N. mikurensis", but were not related to the habitat type. Three hundred fifty eight out of 1078 I. ricinus ticks (33.2%) tested positive for at least one pathogen. Thereof, about 20% (71/358) were carrying two or three different potentially disease-causing agents. Using next generation sequencing, we could detect true pathogens, tick symbionts and organisms of environmental or human origin in ten selected samples.ConclusionsOur data document the presence of pathogens in the (sub-) urban I. ricinus tick population in Switzerland, with carrier rates as high as those in rural regions. Carriage of multiple pathogens was repeatedly observed, demonstrating the risk of acquiring multiple infections as a consequence of a tick bite.Electronic supplementary materialThe online version of this article (10.1186/s13071-017-2500-2) contains supplementary material, which is available to authorized users.
Angiogenesis and vascular remodeling are driven by extensive endothelial cell movements. Here, we present in vivo evidence that endothelial cell movements are associated with oscillating lamellipodia-like structures, which emerge from cell junctions in the direction of cell movements. High-resolution time-lapse imaging of these junction-based lamellipodia (JBL) shows dynamic and distinct deployment of junctional proteins, such as F-actin, VE-cadherin and ZO1, during JBL oscillations. Upon initiation, F-actin and VE-cadherin are broadly distributed within JBL, whereas ZO1 remains at cell junctions. Subsequently, a new junction is formed at the front of the JBL, which then merges with the proximal junction. Rac1 inhibition interferes with JBL oscillations and disrupts cell elongation—similar to a truncation in ve-cadherin preventing VE-cad/F-actin interaction. Taken together, our observations suggest an oscillating ratchet-like mechanism, which is used by endothelial cells to move over each other and thus provides the physical means for cell rearrangements.
Junction-based lamellipodia drive endothelial cell rearrangements in vivo via a 1VE-cadherin/F-actin based oscillatory ratchet mechanism 2 3 4 5 6 Abstract 21 22Angiogenesis and vascular remodeling are driven by a wide range of endothelial cell 23 behaviors, such as cell divisions, cell movements, cell shape and polarity changes. To 24 decipher the cellular and molecular mechanism of cell movements, we have analyzed 25 the dynamics of different junctional components during blood vessel anastomosis in 26 vivo. We show that endothelial cell movements are associated with oscillating 27 lamellipodia-like structures, which are orientated in the direction of these movements. 28These structures emerge from endothelial cell junctions and we thus call them junction-29 based lamellipodia (JBL). High-resolution time-lapse imaging shows that JBL are 30 formed by F-actin based protrusions at the front end of moving cells. These protrusions 31 also contain diffusely distributed VE-cadherin, whereas the junctional protein ZO-1 32 (Zona occludens 1) remains at the junction. Subsequently, a new junction is formed at 33 the front of the JBL and the proximal junction is pulled towards the newly established 34 distal junction. JBL function is highly dependent on F-actin dynamics. Inhibition of F-35 actin polymerization prevents JBL formation, whereas Rac-1 inhibition interferes with 36 JBL oscillations. Both interventions disrupt endothelial junction formation and cell 37 elongation. To examine the role of VE-cadherin (encoded by cdh5 gene) in this process, 38we generated a targeted mutation in VE-cadherin gene (cdh5 ubs25 ), which prevents VE-39 cad/F-actin interaction. Although homozygous ve-cadherin mutants form JBL, these 40 JBL are less dynamic and do not promote endothelial cell elongation. Taken together, 41 our observations suggest a novel oscillating ratchet-like mechanism, which is used by 42 endothelial cells to move along or over each other and thus provides the physical means 43 for cell rearrangements. 44 45 46 Introduction 47 Organ morphogenesis is driven by a wealth of tightly orchestrated cellular behaviors, 48 which ensure proper organ assembly and function. The cardiovascular system is one of 49 the most ramified vertebrate organs and is characterized by an extraordinary plasticity. 50 It forms during early embryonic development, and it expands and remodels to adapt to 51 the needs of the growing embryo. In adult life, this plasticity allows flexible responses, 52 for example, during inflammation and wound healing 1,2 . 53 54 At the cellular level, blood vessel morphogenesis and remodeling are accomplished by 55 endothelial cell behaviors including cell migration, cell rearrangement and cell shape 56 changes 3-5 . This repertoire of dynamic behaviors allows endothelial cells to rapidly 57 respond to different contextual cues, for example during angiogenic sprouting, 58anastomosis, diapedesis or regeneration. In particular, it has been shown that 59 endothelial cells are very motile, not only during sprouting, but ...
Vascular network formation requires the fusion of newly formed blood vessels and the emergence of a patent lumen between the newly established connections so that blood flow can start. Lumen formation has been shown to depend on the late endosomal/lysosomal pathway in various organs of animal tubular systems. Here, we identified a late endosomal/lysosomal vesicular fraction (Rab7/Lamp2) in early zebrafish angiogenic sprouts, which appears to contribute to apical membrane growth during lumen formation. To study the effect of the late endocytic pathway on vascular development, we generated mutant alleles for all threerab7genes in zebrafish (rab7a, rab7ba, rab7bb). Allrab7genes are expressed in wild-type zebrafish and we did not detect any compensatory effects by the otherrab7isoforms in single knockout mutants, which were all viable. Only the triple mutant was lethal suggesting some functional redundancy. However, the differentrab7isoforms fulfil also at least partially independent functions because eggs laid from mothers lacking tworab7(rab7a and/or rab7bb). showed reduced survival and contained enlarged yolk granules, suggesting maternal contribution of these tworab7. Finally, we observed minor effects on lumen formation in embryos which still express one copy ofrab7. Our results support the notion that the late endocytic/lysosomal compartment contributes to lumen expansion.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.