https://www.cell.com/partod/pdf/0169-4758(90)90349-9.pdf

Immune mechanisms in trematode-snail interactions

Differential transcriptomic responses of Biomphalaria glabrata (Gastropoda, Mollusca) to bacteria and metazoan parasites, Schistosoma mansoni and Echinostoma paraensei (Digenea, Platyhelminthes)

Publisher Summary This chapter describes how schistosomes profit from stress responses they elicit in their hosts. The complex life cycle of trematodes comprises at least two hosts—that is, one or more intermediate hosts and a definitive host. The parasitic worms that cause schistosomiasis (bilharzia) in man belong to these trematodes (genus Schistosoma ). Asexual multiplication occurs in the intermediate hosts (freshwater snails), whereas the parasites reach sexual maturity in the definitive hosts (man or other mammals). The major problems which schistosomes have to overcome during their life cycle are (1) they have to find compatible hosts to penetrate their skin and tissue, (2) they have to adapt to environmental stress induced by changes of physicochemical factors, (3) they have to evade immune attacks in their hosts, and (4) they have to obtain energy and space within their hosts to grow and reproduce prior to transmission. Apart from mechanical damage, interference of schistosomes with regulatory mechanisms in their host has to be mediated by parasite components of the parasite–host interface exposed to elements of these regulatory systems or by products secreted into the host.

How schistosomes profit from the stress responses they elicit in their hosts.

Brown ring disease (BRD) is a shell disease caused by Vibrio tapetis. This pathogen disturbs the periostracal lamina causing the appearance of a brown conchiolin deposit on the inner face of the shell, within the extrapallial space. Although differences in resistance to BRD have been documented, their relationship to possible defense functions has never been investigated. In this study, flow cytometry was used to analyze cellular parameters in asymptomatic and experimentally infected Ruditapes philippinarum from France and the west coast of the USA. Parallel analyses were made on Ruditapes decussatus, the native European clam, which is highly resistant to BRD. In the haemolymph and extrapallial fluid of animals without BRD, total haemocyte counts, the percentage of granulocytes, and the phagocytic activity against latex beads or V. tapetis by the haemocytes were significantly higher in American R. philippinarum than in French R. philippinarum. In most cases, levels in R. decussatus were the highest of all three groups. Four weeks following challenge with V. tapetis, BRD prevalence reached 52 in American clams and 100% in French specimens, but only 37% in R. decussatus. In symptomatic animals, phagocytosis of V. tapetis increased significantly in the resistant species of clam, R. decussatus, was unchanged in US clams, and decreased significantly in FR specimens when compared to asymptomatic individuals from each population. Ingestion of V. tapetis by haemocytes in the extrapallial fluid, which is in contact with the periostracal lamina, could be the main defense mechanism used to counter the pathogen. Our results suggest that resistance to BRD may well be related to the concentration of granular haemocytes and the phagocytic activity of haemocytes.

Haemocyte parameters associated with resistance to brown ring disease in Ruditapes spp. clams.

Many parasites develop in invertebrate hosts that possess internal defense systems (IDS) that vigorously defined self-integrity Invertebrates apparently do not produce a large diversity of finely tuned immunorecognition molecules but rather rely on recognition of patterns As a consequence, requirements for immune evasion are likely to be fundamentally different in such hosts Although parasites of invertebrates certainly employ diverse tactics to evade host IDS, this review focuses on parasite-mediated interference with the structural and functional integrity of host hemocytes and argues that this is a common strategy of immune evasion Parasites mediating such effects on host hemocytes are termed suppressors In some cases, interference is mediated by mutualistic symbionts carried by the suppressors Hemocytes from infected hosts exhibit diminished adherence to substrates, impaired spreading ability, and reduced ability to participate in phagocytosis or encapsulation reactions As a result of the action of suppressors, the host's vulnerability to opportunistic parasites is increased, a phenomenon termed acquired susceptibility A strategy of interference is therefore risky, particularly for suppressors with relatively long development times As a result, suppressors may provoke either a partial generalized interference or a selective interference with host IDS function, actively contribute to protection of the host to discourage growth of opportunists (termed parasite-mediated internal defense), or induce compensatory host responses that protect the host but that do not jeopardize their own development Some parasites consistently colonize previously infected hosts and seem to be specialized opportunists

On being a parasite in an invertebrate host: a short survival course.

The phagocytic activity of hemocytes from 6-8-mm M-line Biomphalaria glabrata snails was studied in an in vitro assay using glutaraldehyde-fixed sheep erythrocytes (SRBC) as target cells. For individual snails, the percentage of hemocytes ingesting SRBC during a 1-hr interval, termed the phagocytic activity index (PAI), was determined. Hemocytes from snails infected for 1 day with Echinostoma paraensei had a slightly elevated PAI, but at both 8 and 30 days postexposure (DPE), hemocytes from infected snails had a significantly lower PAI than controls. Hemocytes taken from snails at 8 DPE also had a low PAI using rabbit erythrocytes and yeast as target cells. The low PAI at 8 DPE is attributed to the presence of large numbers of poorly spreading hemocytes with low phagocytic activity. Hemocytes from snails with 30-day infections were well spread but nonetheless had a low PAI. The presence of plasma from 8-day infected snails did not alter the PAI of hemocytes from control snails, nor was the PAI of hemocytes from infected snails changed by plasma from control snails. SRBC preincubated for 60 min in plasma from various groups of M-line snails did not elicit an increase in PAI when presented to hemocytes from control snails; in some cases, as with plasma from 6-8-mm control snails, such preincubation significantly reduced the PAI below levels obtained using SRBC preincubated in culture medium. As compared to hemocytes from snails with normally developing, 8-day-old intraventricular sporocysts (IS), hemocytes from snails exposed to infection but subsequently lacking IS had a significantly higher PAI.(ABSTRACT TRUNCATED AT 250 WORDS)

Shinichi Noda

Papers

Phagocytic activity of hemocytes of M-line Biomphalaria glabrata snails: effect of exposure to the trematode Echinostoma paraensei.