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    Disruption of haemocyte function by exposure to cytochalasin b or nocodazole increases the susceptibility of Galleria mellonella larvae to infection


    Banville, Nessa and Fallon, John and McLoughlin, Kirstin and Kavanagh, Kevin (2011) Disruption of haemocyte function by exposure to cytochalasin b or nocodazole increases the susceptibility of Galleria mellonella larvae to infection. Microbes and Infection, 13. pp. 1191-1198. ISSN 1286-4579

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    Abstract

    Administration of non-toxic concentrations (10 mM) of cytochalasin b and nocodazole to larvae of Galleria mellonella increased their susceptibility to infection by the yeast Candida albicans. These agents were found to inhibit the process of phagocytosis and to reduce the killing ability of haemocytes. In addition, both cytochalasin b and nocodazole reduced the release of antimicrobial peptides (e.g. apolipophorin 3) and enzymes (e.g. serine protease) from PMA stimulated haemocytes. Rhodamine coupled phalloidin staining revealed reduced F-actin formation in haemocytes treated with nocodazole or cytochalasin b. By disrupting the formation of F-actin cytochalasin b and nocodazole have the ability to retard the function of haemocytes, in the same manner as they affect mammalian neutrophils, and thus increase the susceptibility of larvae to infection. The results presented here demonstrate that haemocytes are sensitive to inhibition by nocodazole and cytochalasin b, in a similar manner to neutrophils, thus highlighting another similarity between both cell types and so increasing the attractiveness of using insects as alternative models to the use of mammals for in vivo pathogen or drug screening.

    Item Type: Article
    Keywords: Cytochalasin b; Galleria; Haemocyte; Mini-host; Nocodazole; Neutrophil;
    Academic Unit: Faculty of Science and Engineering > Biology
    Item ID: 4186
    Depositing User: Dr. Kevin Kavanagh
    Date Deposited: 04 Feb 2013 15:01
    Journal or Publication Title: Microbes and Infection
    Publisher: Elsevier
    Refereed: Yes
    URI:

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