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Coakley, G.* ; Volpe, B.* ; Bouchery, T.* ; Shah, K.* ; Butler, A.* ; Geldhof, P.* ; Hatherill, M.* ; Horsnell, W.* ; Esser-von Bieren, J. ; Harris, N.L.*

Immune serum-activated human macrophages coordinate with eosinophils to immobilize Ascaris suum larvae.

Parasite Immunol. 42:e12728 (2020)
Publ. Version/Full Text Postprint Research data DOI PMC
Open Access Green
Helminth infection represents a major health problem causing approximately 5 million disability-adjusted life years worldwide. Concerns that repeated anti-helminthic treatment may lead to drug resistance render it important that vaccines are developed but will require increased understanding of the immune-mediated cellular and antibody responses to helminth infection. IL-4 or antibody-activated murine macrophages are known to immobilize parasitic nematode larvae, but few studies have addressed whether this is translatable to human macrophages. In the current study, we investigated the capacity of human macrophages to recognize and attack larval stages of Ascaris suum, a natural porcine parasite that is genetically similar to the human helminth Ascaris lumbricoides. Human macrophages were able to adhere to and trap A suum larvae in the presence of either human or pig serum containing Ascaris-specific antibodies and other factors. Gene expression analysis of serum-activated macrophages revealed that CCL24, a potent eosinophil attractant, was the most upregulated gene following culture with A suum larvae in vitro, and human eosinophils displayed even greater ability to adhere to, and trap, A suum larvae. These data suggest that immune serum-activated macrophages can recruit eosinophils to the site of infection, where they act in concert to immobilize tissue-migrating Ascaris larvae.
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Publication type Article: Journal article
Document type Review
Corresponding Author
Keywords Antibodies ; Ascariasis ; Eosinophils ; Helminth ; Immune Serum ; Macrophage; Trichinella-spiralis; Protective Immunity; Th2 Cytokines; In-vitro; Lumbricoides; Neutrophils; Resistance; Receptor; Infections; Expression
ISSN (print) / ISBN 0141-9838
e-ISSN 1365-3024
Quellenangaben Volume: 42, Issue: 7, Pages: , Article Number: e12728 Supplement: ,
Publisher Blackwell
Publishing Place Oxford
Non-patent literature Publications
Reviewing status Peer reviewed