Cited by 21Parasitic Diseases Research and TreatmentHelminth infection and controlParasites and Host Interactions

Dirofilaria immitis and Wolbachia-derived antigens: Its effect on endothelial mammal cells

Simón, F., Morchón, R., Rodríguez-Barbero, A., López-Belmonte, J., Grandi, G., Genchi, C.·2008·Veterinary Parasitology

Abstract

Antigens of both Dirofilaria immitis and Wolbachia symbiont bacteria are implicated in the inflammatory pathology of heartworm infection. The aim of the present study was to compare the stimulatory capacity of in vitro cultures of vascular endothelial cells by the adult somatic antigens of D. immitis (DiSA) and the recombinant form of the Wolbachia surface protein (rWSP), during the first 24h of stimulation. Our results indicate a different stimulatory activity of the two antigens. Both the DiSA and rWSP stimulate the production of the enzymes responsible of the arachidonic acid metabolism, cyclooxygenase-2, 5-lipoxygenase (5-LO), and leukotriene B4. Only DiSA stimulates the production of prostaglandin E2. Related to the adhesion molecules, the DiSA stimulates the expression of intercellular adhesion molecule-1 (ICAM-1) and platelet endothelial cell adhesion molecule-1 (PECAM-1), whereas rWSP stimulates ICAM-1, PECAM-1, and vascular cell adhesion molecule-1 (VCAM-1). Expression of E-cadherin and vascular endothelial growth factor also were stimulated by rWSP. Neither of the two antigens altered the basic physiological mechanisms of endothelial cells, such as cell proliferation, cell cycle, or apoptosis. The biological and pathological significance of these finding are discussed.

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Crossref · 10.1016/j.vetpar.2008.09.010

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  • Symbiotic bacteria stimulate proinflammatory eicosanoid production in vascular endothelium.

    “which suggests that symbiotic bacteria stimulate proinflammatory eicosanoid production in the vascular endothelium.”
  • WSP-stimulated vascular endothelial cell cultures show increased expression of COX2, 5-LO, TxB2, and LTB4.

    “Vascular endothelial cell cultures stimulated with WSP exhibit significant increases in the expression levels of enzymes responsible for eicosanoid synthesis (cyclooxygenase 2 [COX2] and 5-lipooxygenase [LO]) and of TxB2 and LTB4 (296, 394)”
  • Vascular endothelium is altered during D. immitis infection, undergoing inflammation and endothelial cell disorganization.

    “the vascular endothelium is altered during D. immitis infection, undergoing inflammation and endothelial cell disorganization (394).”
  • Many molecules increased by Wolbachia antigens are also produced by endothelial cell cultures treated with DiSA.

    “many of these molecules are also produced by endothelial cell cultures treated with DiSA (394)”

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Authors
Simón, F., Morchón, R., Rodríguez-Barbero, A., López-Belmonte, J., Grandi, G., & Genchi, C.
Affiliations
  • Universidad de Salamanca (ES)
  • University of Milan (IT)
Corresponding author
Simón, F.
Venue
Veterinary Parasitology
Publisher
Elsevier BV
Published
2008-12
Volume
158
Issue
3
Pages
223-231
ISSN
0304-4017 (ISSN-L)
OpenAlex
W2068200009
Cited by
21
References
31
Citations by year
2026: 1 · 2025: 1 · 2024: 1 · 2023: 2 · 2022: 2 · 2019: 1 · 2017: 1 · 2014: 1 · 2012: 2
FWCI
1.93
Type
journal article
Language
en
Open access
closed
Locations
  • Veterinary Parasitology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Infectious Diseases › Parasitic Diseases Research and Treatment
  • Health Sciences › Veterinary › Small Animals › Helminth infection and control
  • Life Sciences › Immunology and Microbiology › Parasitology › Parasites and Host Interactions
Keywords
Dirofilaria immitis, Wolbachia, heartworm infection, endothelial cells, vascular endothelial growth factor, arachidonic acid metabolism, cyclooxygenase-2, 5-lipoxygenase, leukotriene B4, prostaglandin E2, adhesion molecules, ICAM-1, CD31, VCAM-1, E-cadherin, Wolbachia surface protein, inflammatory pathology
MeSH terms
Animals, Antigens, Helminth, Cells, Cultured, Dirofilaria immitis, Endothelium, Vascular, Humans, Inflammation, Membrane Proteins, Intercellular Adhesion Molecule-1, Vascular Cell Adhesion Molecule-1, Platelet Endothelial Cell Adhesion Molecule-1, Wolbachia, Vascular Endothelial Growth Factor A, Endothelial Cells

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