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Cited by 28Parasitic Diseases Research and TreatmentParasites and Host InteractionsHelminth infection and control

Dirofilaria immitis: Do filarial cyclooxygenase products depress endothelium-dependent relaxation in the in vitro rat aorta?

Kaiser, Lana, Lamb, Victoria L., Tithof, Patricia K., Gage, Douglas A., Chamberlin, Beverly A., Watson, J.T., Williams, Jeffrey F.·1992·Experimental Parasitology
DOI 10.1016/0014-4894(92)90175-a
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Abstract

Endothelial cells modulate the function of their underlying smooth muscle. Thus, altered endothelial behavior could be important in the pathogenesis of vascular and lymphatic diseases, including human and animal filariasis. Endothelium-dependent relaxation is depressed in both in vivo canine femoral artery of dogs infected with Dirofilaria immitis and in vitro rat aorta exposed to adult D. immitis. The experiments reported here were designed to determine if filarial cyclooxygenase products could depress endothelium-dependent relaxation in vitro. Pretreatment of the parasites, but not the vascular ring, with either indomethacin or aspirin, prevented filarial-induced depression of relaxation. Analysis of heartworm-conditioned medium by gas chromatography--mass spectrometry revealed two peaks in the biologically active medium that were not present in the control. One peak had a retention time and chromatographic profile characteristic of derivatized PGD2 standard, and the other was not identified. Incubation of the vascular ring with PGD2 mimicked filarial-induced depression of endothelium-dependent relaxation at low, but not high, concentrations of acetylcholine. Thus, filarial PGD2 may be involved in altered endothelium-dependent relaxation seen in heartworm-infected dogs.

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  • Filarial cyclooxygenase products such as PGD2 induce depression of endothelium-dependent relaxation at low but not high acetylcholine concentrations.

    “products of the cyclooxygenase pathway in filariae, such as prostaglandin D2 (PGD2), induce the depression of endothelium-dependent relaxation at low, but not at high, acetylcholine concentrations (192).”

    From Human and animal dirofilariasis: The emergence of a zoonotic mosaic (2012) · cites this paper as [192]

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Authors
Kaiser, L., Lamb, V. L., Tithof, P. K., Gage, D. A., Chamberlin, B. A., Watson, J. T., & Williams, J. F.
Affiliations
Michigan State University (US)
ORCID
Williams, Jeffrey F.
Venue
Experimental Parasitology
Publisher
Elsevier BV
Published
1992-09
Volume
75
Issue
2
Pages
159-167
ISSN
0014-4894 (ISSN-L)
DOI
10.1016/0014-4894(92)90175-a
OpenAlex
W2049833374
Cited by
28
References
15
Citations by year
2025: 1 · 2017: 1 · 2015: 2 · 2012: 1
FWCI
1.42
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Experimental Parasitology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5k08hl001842-05, 5p41rr000480-28, 5r01hl025779-13)
  • National Heart, Lung, and Blood Institute (HL-25779, HL-01842)
  • National Center for Research Resources (RR 00480)
Topics
  • Health Sciences › Medicine › Infectious Diseases › Parasitic Diseases Research and Treatment
  • Life Sciences › Immunology and Microbiology › Parasitology › Parasites and Host Interactions
  • Health Sciences › Veterinary › Small Animals › Helminth infection and control
Keywords
Dirofilaria immitis, cyclooxygenase products, prostaglandin D2, endothelium-dependent relaxation, endothelial dysfunction, rat aorta, indomethacin, aspirin, acetylcholine, filariasis, canine heartworm disease
MeSH terms
Acetylcholine, Animals, Aorta, Thoracic, Aspirin, Dirofilaria immitis, Endothelium, Vascular, Female, Indomethacin, Male, Rats, Inbred Strains, Vasodilation, Prostaglandin D2, Rats, In Vitro Techniques

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