Abstract
AimsES‐62 is a well‐studied anti‐inflammatory molecule secreted by L4‐adult stage Acanthocheilonema viteae. We maintain the life cycle of A viteae using Meriones libycus as the definitive host. Here, we investigated whether the full life cycle could be maintained, and functional ES‐62 produced, in a related jird species—Meriones shawi.Methods and ResultsAdult worms were produced in comparable numbers in the two species, but very few microfilariae (MF) were observed in the M shawi bloodstream. M shawi ES‐62 produced ex vivo was functional and protective in a mouse model of arthritis. Myeloid‐derived cells from naïve and infected jirds of both species were compared with respect to ROS production and osteoclast generation, and some differences between the two species in both the absence and presence of infection were observed.ConclusionsThe life cycle of A viteae cannot be successfully completed in M shawi jirds but L3 stage worms develop to adulthood and produce functional ES‐62. Preliminary investigation into jird immune responses suggests that infection can differentially modulate myeloid responses in the two species. However, species‐specific reagents are required to understand the complex interplay between A viteae and its host and to explain the lack of circulating MF in infected M shawi jirds.
Highlights
Filarial nematodes are a group of arthropod-transmitted parasites of vertebrates
While we were not able to detect cytokine production by jird BM-derived macrophages (BMMs) due to lack of reagents, we found that infection of M libycus significantly and stably decreased the subsequent Reactive oxygen species (ROS) production by BMMs when stimulated with LPS or CpG (Figure 2D)
We investigated whether osteoclast (OC) differentiation was altered by helminth infection in these jirds as OCs are myeloid-derived Bone marrow (BM) cells that rely on high ROS levels for differentiation and survival and which ES-62 targets in its protection against joint disease.[11]
Summary
Filarial nematodes are a group of arthropod-transmitted parasites of vertebrates. Adult worms, depending on species, are found in various tissues and body cavities of their definitive hosts and produce microfilariae (MF) that circulate in the bloodstream or migrate through the tissues to enable transmission. Filarial nematodes often induce lifelong infections, due to their ability to modulate their host's immune response to promote their own survival while at the same time, limiting host pathology This immunoregulation is thought to be driven by the secretion of bioactive molecules by the nematodes.[1] One of the best characterized secreted molecules is ES-62, a phosphorylcholine-containing glycoprotein produced by Acanthocheilonema viteae. Despite having extensively studied the effect of ES-62 in mouse models of disease, we know very little about how the molecule interacts with the immune system of a receptive host Work in this area has been hampered by the lack of jird-specific reagents required to investigate the effect of ES-62 on specific immune cell populations; we were able to study the effects of the nematode product on certain functional responses of host cells.
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