Parasitic manipulation and neuroinflammation: Evidence from the system Microphallus papillorobustus (Trematoda) - Gammarus (Crustacea)
Identifieur interne : 000177 ( France/Analysis ); précédent : 000176; suivant : 000178Parasitic manipulation and neuroinflammation: Evidence from the system Microphallus papillorobustus (Trematoda) - Gammarus (Crustacea)
Auteurs : Simone Helluy [États-Unis] ; Frederic Thomas [Canada, France]Source :
- Parasites & Vectors [ 1756-3305 ] ; 2010.
Abstract
Neuropathological consequences of neuroinflammatory processes have been implicated in a wide range of diseases affecting the central nervous system (CNS). Glial cells, the resident immune cells of the CNS, respond to tissue injury by releasing proinflammatory cytokines and free radicals such as nitric oxide. We explored the possibility that neuroimmune responses are involved in parasitic manipulation of host behavior in a trematode-crustacean association. The cerebral larva of the flatworm
Immunocytochemical experiments followed by confocal microscopy were performed to study the distribution of glutamine synthetase, a glial cell marker, and nitric oxide synthase in the brain of gammarids. Astrocyte-like glia and their processes were abundant at the surface of the parasites while levels of nitric oxide synthase were elevated at the host-parasite interface in the brain of gammarids harboring mature cerebral larvae and demonstrating altered behavior.
Taken together these results lend support to the neuroinflammation hypothesis whereby a chronic CNS specific immune response induced by the parasite plays a role in the disruption of neuromodulation, neuronal integrity, and behavior in infected hosts.
Url:
DOI: 10.1186/1756-3305-3-38
PubMed: 20398322
PubMed Central: 2874546
Affiliations:
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PMC:2874546Le document en format XML
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<sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Parasitic manipulation and neuroinflammation: Evidence from the system <italic>Microphallus papillorobustus </italic>
(Trematoda) - <italic>Gammarus </italic>
(Crustacea)</title>
<author><name sortKey="Helluy, Simone" sort="Helluy, Simone" uniqKey="Helluy S" first="Simone" last="Helluy">Simone Helluy</name>
<affiliation wicri:level="1"><nlm:aff id="I1">Department of Biological Sciences, Wellesley College, Wellesley, MA 02481, USA</nlm:aff>
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<author><name sortKey="Thomas, Frederic" sort="Thomas, Frederic" uniqKey="Thomas F" first="Frederic" last="Thomas">Frederic Thomas</name>
<affiliation wicri:level="1"><nlm:aff id="I2">Institut de recherche en biologie végétale, Département de sciences biologiques, Université de Montréal, 4101, rue Sherbrooke est, Montréal, Québec, H1X 2B2, Canada</nlm:aff>
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<series><title level="j">Parasites & Vectors</title>
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<front><div type="abstract" xml:lang="en"><sec><title>Background</title>
<p>Neuropathological consequences of neuroinflammatory processes have been implicated in a wide range of diseases affecting the central nervous system (CNS). Glial cells, the resident immune cells of the CNS, respond to tissue injury by releasing proinflammatory cytokines and free radicals such as nitric oxide. We explored the possibility that neuroimmune responses are involved in parasitic manipulation of host behavior in a trematode-crustacean association. The cerebral larva of the flatworm <italic>Microphallus papillorobustus </italic>
alters responses to environmental stimuli - and thus reflex pathways - in the crustacean <italic>Gammarus insensibilis</italic>
, in a way that enhances predation of the crustacean by birds, definitive hosts of the parasite.</p>
</sec>
<sec><title>Results</title>
<p>Immunocytochemical experiments followed by confocal microscopy were performed to study the distribution of glutamine synthetase, a glial cell marker, and nitric oxide synthase in the brain of gammarids. Astrocyte-like glia and their processes were abundant at the surface of the parasites while levels of nitric oxide synthase were elevated at the host-parasite interface in the brain of gammarids harboring mature cerebral larvae and demonstrating altered behavior.</p>
</sec>
<sec><title>Conclusion</title>
<p>Taken together these results lend support to the neuroinflammation hypothesis whereby a chronic CNS specific immune response induced by the parasite plays a role in the disruption of neuromodulation, neuronal integrity, and behavior in infected hosts.</p>
</sec>
</div>
</front>
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