Peer-reviewed veterinary case report
How heartworm larvae trigger immune traps in dogs
By Muñoz-Caro, Tamara et al.·Published in Frontiers in immunology·2018·Institute of Parasitology, Germany·View original on PubMed →
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Original publication title: Microfilariae and Third-Stage Larvae Induce Canine NETosis Resulting in Different Types of Neutrophil Extracellular Traps.
- Species:
- dog
Plain-English summary
A study found that heartworm larvae can trigger immune responses in dogs, specifically causing neutrophils (a type of white blood cell) to form structures called neutrophil extracellular traps (NETs). These traps help to entrap the larvae but do not kill them. Both the microfilariae (first-stage larvae) and third-stage larvae (L3) were effective at inducing these traps, although they produced different types of NETs. This research highlights how heartworm can affect a dog's immune system, but it does not provide a direct treatment outcome for infected dogs.
People also search for: heartworm disease in dogs · symptoms of heartworm in dogs · treatment for heartworm in dogs
Abstract
Heartworm disease is a zoonotic vector-borne disease caused bymainly affecting canids. Infectious third-stage larvae (L3) are transmitted to the definitive hostsculicid mosquitoes; adult nematodes reside in the pulmonary arteries and in the right heart releasing unsheathed first-stage larvae (microfilariae) into the bloodstream leading to chronic and sometimes fatal disease. So far, early innate immune reactions triggered by these differentstages in the canine host have scarcely been investigated. Therefore,microfilariae and L3 were analyzed for their capacity to induce neutrophil extracellular traps (NETs) in canine polymorphonuclear neutrophils (PMN). Overall, scanning electron microscopy analysis revealed both larval stages as strong inducers of canine NETosis. Co-localization of PMN-derived extracellular DNA with granulocytic histones, neutrophil elastase, or myeloperoxidase in parasite-entrapping structures confirmed the classical characteristics of NETosis. Quantitative analyses showed that both larval stages triggered canine NETs in a time-dependent but dose-independent manner. Moreover, parasite-induced NET formation was not influenced by the parasites viability since heat-inactivated microfilariae and L3 also induced NETs. In addition, parasite/PMN confrontation promoted significant entrapment but not killing of microfilariae and L3. Both, NETosis and larval entrapment was significantly reversedDNase I treatments while treatments with the NADPH oxidase inhibitor diphenyleneiodonium failed to significantly influence these reactions. Interestingly, different types of NETs were induced by microfilariae and L3 since microfilarial stages merely induced spread and diffuse NETs while the larger L3 additionally triggered aggregated NET formation.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/29867950/