Increased Endothelial Cell-Leukocyte Interaction in Murine Schistosomiasis: Possible Priming of Endothelial Cells by the Disease
Open Access
- 10 August 2011
- journal article
- research article
- Published by Public Library of Science (PLoS) in PLOS ONE
- Vol. 6 (8), e23547
- https://doi.org/10.1371/journal.pone.0023547
Abstract
Schistosomiasis is an intravascular parasitic disease associated with inflammation. Endothelial cells control leukocyte transmigration and vascular permeability being modulated by pro-inflammatory mediators. Recent data have shown that endothelial cells primed in vivo in the course of a disease keep the information in culture. Herein, we evaluated the impact of schistosomiasis on endothelial cell-regulated events in vivo and in vitro. The experimental groups consisted of Schistosoma mansoni-infected and age-matched control mice. In vivo infection caused a marked influx of leukocytes and an increased protein leakage in the peritoneal cavity, characterizing an inflamed vascular and cellular profile. In vitro leukocyte-mesenteric endothelial cell adhesion was higher in cultured cells from infected mice as compared to controls, either in the basal condition or after treatment with the pro-inflammatory cytokine tumor necrosis factor (TNF). Nitric oxide (NO) donation reduced leukocyte adhesion to endothelial cells from control and infected groups; however, in the later group the effect was more pronounced, probably due to a reduced NO production. Inhibition of control endothelial NO synthase (eNOS) increased leukocyte adhesion to a level similar to the one observed in the infected group. Besides, the adhesion of control leukocytes to endothelial cells from infected animals is similar to the result of infected animals, confirming that schistosomiasis alters endothelial cells function. Furthermore, NO production as well as the expression of eNOS were reduced in cultured endothelial cells from infected animals. On the other hand, the expression of its repressor protein, namely caveolin-1, was similar in both control and infected groups. Schistosomiasis increases vascular permeability and endothelial cell-leukocyte interaction in vivo and in vitro. These effects are partially explained by a reduced eNOS expression. In addition, our data show that the disease primes endothelial cells in vivo, which keep the acquired phenotype in culture.This publication has 41 references indexed in Scilit:
- Nitric oxide modulates the expression of endothelial cell adhesion molecules involved in angiogenesis and leukocyte recruitmentExperimental Cell Research, 2011
- Long-Lasting Priming of Endothelial Cells by Plasma Melatonin LevelsPLOS ONE, 2010
- Effects of nitric oxide on neutrophil influx depends on the tissue: role of leukotriene B4 and adhesion moleculesBritish Journal of Pharmacology, 2009
- Endogenous glucocorticoids control neutrophil mobilization from bone marrow to blood and tissues in non‐inflammatory conditionsBritish Journal of Pharmacology, 2007
- Melatonin inhibits nitric oxide production by microvascular endothelial cells in vivo and in vitroBritish Journal of Pharmacology, 2007
- Coupling eNOS Uncoupling to the Innate Immune ResponseArteriosclerosis, Thrombosis, and Vascular Biology, 2006
- Immunopathogenesis of schistosomiasisImmunological Reviews, 2004
- Serum concentrations of sICAM‐1, sE‐, sP‐ and sL‐selectins in patients with Schistosoma mansoni infection and association with disease severityParasite Immunology, 1998
- Expression of intercellular adhesion molecule-1 and lymphocytefunction-associated antigen-1 in experimental Schistosoma mansoni infection and in synchronous periparticular hepatic granulomas in mice: immunohistochemistry, confocal laser scanning microscopy, and immunoelectron microscopyZeitschrift für Parasitenkunde, 1997
- Observations on two biological races of Schistosoma mansoniMemórias do Instituto Oswaldo Cruz, 1981