Effect of a hemiuroid trematode on the hemocyte immune parameters of the cockle Anadara trapezia Cécile Dang a, * , Thomas H. Cribb a , Geoffrey Osborne b, c , Minami Kawasaki a , Anne-Sophie Bedin b , Andrew C. Barnes a a The University of Queensland, School of Biological Science and Centre for Marine Science, Brisbane, QLD 4072, Australia b Queensland Brain Institute, The University of Queensland, St Lucia, QLD 4072, Australia c The Australian Institute for Bioengineering and Nanotechnology, The University of Queensland, St Lucia, QLD 4072, Australia article info Article history: Received 21 August 2012 Received in revised form 25 June 2013 Accepted 8 July 2013 Available online 16 July 2013 Keywords: Anadara trapezia Cellular immunity Trematode Hemiuroid Immunomodulation abstract When a trematode parasite penetrates a potential molluscan host, it has to circumvent the host’s internal defense system. In molluscs, the primary effector cells of this system are the hemocytes which orches- trate many of the cellular and humoral immune functions. Survival of the parasite can occur only in the absence of a successful immune response, and continued development only if the host is physiologically suitable. This study investigated hemocytic response against asexual stages of a hemiuroid trematode by its host, the marine bivalve Anadara trapezia. Hemocyte characteristic (type, morphology) and function (mortality, phagocytosis and oxidative activity) were analyzed by flow cytometry in parasitized and non- parasitized cockles. A. trapezia possesses two types of hemocytes: amebocytes and erythrocytes. Analysis of histological section showed that there was no host hemocytic response around hemiuroid sporocysts. The infection induced a significant increase of the total circulating hemocytes with a higher proportion of erythrocytes relative to amebocytes, coupled with a lower phagocytosis rate and a statistically non- significant decrease of the intracellular oxidative activity. No significant differences were observed in hemocyte size and complexity, mortality, or phagocytic capacity. Our results indicate that in A. trapezia, hemiuroids modulate the immune response by increasing the number of circulating hemocytes and decreasing phagocytosis. Ó 2013 Elsevier Ltd. All rights reserved. 1. Introduction Molluscs possess a typical invertebrate immune system con- sisting of both cellular and humoral components that cooperate in the recognition and elimination of non-self entities [1,2]. The hu- moral activity is based on the production of soluble effector mol- ecules that increase and regulate antimicrobial activities [1,2], while cellular defenses include phagocytosis and encapsulation [3,4]. Bivalve hemocytes are found in the circulating hemolymph of molluscs and are the primary effector cells, coordinating many immunological functions [5,6]. Killing of phagocytosed small or- ganisms or encapsulated larger organisms occurs by hemocyte- mediated cytotoxicity [7], using both non-oxidative and oxidative killing mechanisms. When a trematode penetrates a potential molluscan host, its fate is dependent on both parasite infectivity and host suscepti- bility. It must evade the host’s internal defence system [8]. Survival of the parasite can occur only in the absence of an effective immune response, and continued development is possible only if the host is physiologically suitable [9]. Interestingly, trematode parasites can evade elimination by hemocytes in fully immuno-competent compatible hosts, but the precise mechanisms of this phenome- non are still unclear [9,10]. Although knowledge of the physiolog- ical, biochemical, and molecular aspects of hosteparasite interactions is increasing in a few well-developed model systems, the mechanisms underlying trematode susceptibility or resistance in molluscs remain unclear [10]. In a susceptible host, trematodes may successfully establish either because of non-recognition of the parasite by the host de- fense due to the presence of host-like or host-derived molecules on the parasite surface (Van Der Knaap and Meuleman 1986 in Ref. [55]) or by suppressing the anti-parasite defense reactions in the host. Immunosuppression may be implicated when a host infected * Corresponding author. Tel.: þ61 7 3346 7289; fax: þ61 7 3365 4755. E-mail address: c.dang@uq.edu.au (C. Dang). Contents lists available at SciVerse ScienceDirect Fish & Shellfish Immunology journal homepage: www.elsevier.com/locate/fsi 1050-4648/$ e see front matter Ó 2013 Elsevier Ltd. All rights reserved. http://dx.doi.org/10.1016/j.fsi.2013.07.010 Fish & Shellfish Immunology 35 (2013) 951e956