ArticleInfection and immunity2005
Loss of complement activation and leukocyte adherence as Nippostrongylus brasiliensis develops within the murine host.
Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- Vaccination against Onchocerca volvulus induces IgG-mediated protective immunity dependent on neutrophils and complement.NPJ vaccines · 2025Article
- Disruption of the C5a/C5aR1 axis confers protection against hookworm infection in lung.Frontiers in immunology · 2024Article
- The liver proteome in a mouse model for Ascaris suum resistance and susceptibility: evidence for an altered innate immune response.Parasites & vectors · 2019Article
- Of dogs and hookworms: man's best friend and his parasites as a model for translational biomedical research.Parasites & vectors · 2018Review
- Eosinophils mediate protective immunity against secondary nematode infection.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Intrathecal activation as a typical immune response within the central nervous system in angiostrongyliasis.The American journal of tropical medicine and hygiene · 2013Review
- A role for eosinophils in the intestinal immunity against infective Ascaris suum larvae.PLoS neglected tropical diseases · 2013Article
- A cross-reactive monoclonal antibody to nematode haemoglobin enhances protective immune responses to Nippostrongylus brasiliensis.PLoS neglected tropical diseases · 2013Article
- Granulocytes in helminth infection -- who is calling the shots?Current medicinal chemistry · 2012Review
- The landscape of human genes involved in the immune response to parasitic worms.BMC evolutionary biology · 2010Article
- Inactivation of the complement anaphylatoxin C5a by secreted products of parasitic nematodes.International journal for parasitology · 2010Article
- FVB/N mice are highly resistant to primary infection with Nippostrongylus brasiliensis.Parasitology · 2009Article
- Role of glycan synthesis in colonization of the mammalian gut by the bacterial symbiont Bacteroides fragilis.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Borrelia burgdorferi binding of host complement regulator factor H is not required for efficient mammalian infection.Infection and immunity · 2007Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Complement activation and C3 deposition on the surface of parasitic helminths may be important for recruitment of leukocytes and for damage to the target organism via cell-mediated mechanisms. Inhibition of complement activation would therefore be advantageous to parasites, minimizing damage and enhancing migration through tissues. The aim of this study was to determine ex vivo if complement activation by, and leukocyte adherence to, the nematode Nippostrongylus brasiliensis change as the parasite matures and migrates through the murine host. Pathways of activation of complement and the mechanism of adherence of leukocytes were also defined using sera from mice genetically deficient in either C1q, factor B, C1q and factor B, C3, or C4. Substantive deposition of C3 and adherence of eosinophil-rich leukocytes were seen with infective-stage (L3) but not with lung-stage (L4) larvae. Adult intestinal worms had low to intermediate levels of both C3 and leukocyte binding. For L3 and adult worms, complement deposition was principally dependent on the alternative pathway. For lung-stage larvae, the small amount of C3 detected was dependent to similar degrees on both the lectin and alternative pathways. The classical pathway was not involved for any of the life stages of the parasite. These results suggest that in primary infections, the infective stage of N. brasiliensis is vulnerable to complement-dependent attack by leukocytes. However, within the first 24 h of infection, N. brasiliensis acquires the ability to largely avoid complement-dependent immune responses.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.