Abstract
BackgroundHelminth neuroinfections represent a serious health problem, but host immune mechanisms in the nervous tissue often remain undiscovered. This study aims at in vitro characterization of the response of murine astrocytes and microglia exposed to Trichobilharzia regenti which is a neuropathogenic schistosome migrating through the central nervous system of vertebrate hosts. Trichobilharzia regenti infects birds and mammals in which it may cause severe neuromotor impairment. This study was focused on astrocytes and microglia as these are immunocompetent cells of the nervous tissue and their activation was recently observed in T. regenti-infected mice.ResultsPrimary astrocytes and microglia were exposed to several stimulants of T. regenti origin. Living schistosomulum-like stages caused increased secretion of IL-6 in astrocyte cultures, but no changes in nitric oxide (NO) production were noticed. Nevertheless, elevated parasite mortality was observed in these cultures. Soluble fraction of the homogenate from schistosomulum-like stages stimulated NO production by both astrocytes and microglia, and IL-6 and TNF-α secretion in astrocyte cultures. Similarly, recombinant cathepsins B1.1 and B2 triggered IL-6 and TNF-α release in astrocyte and microglia cultures, and NO production in astrocyte cultures. Stimulants had no effect on production of anti-inflammatory cytokines IL-10 or TGF-β1.ConclusionsBoth astrocytes and microglia are capable of production of NO and proinflammatory cytokines IL-6 and TNF-α following in vitro exposure to various stimulants of T. regenti origin. Astrocytes might be involved in triggering the tissue inflammation in the early phase of T. regenti infection and are proposed to participate in destruction of migrating schistosomula. However, NO is not the major factor responsible for parasite damage. Both astrocytes and microglia can be responsible for the nervous tissue pathology and maintaining the ongoing inflammation since they are a source of NO and proinflammatory cytokines which are released after exposure to parasite antigens.Electronic supplementary materialThe online version of this article (doi:10.1186/s13071-016-1869-7) contains supplementary material, which is available to authorized users.
Highlights
Helminth neuroinfections represent a serious health problem, but host immune mechanisms in the nervous tissue often remain undiscovered
In case of astrocyte cultures, significant differences were noticed among the groups (K-W test: χ2 = 36.00, df = 5, P < 0.001; Fig. 2, black bars)
In supernatants of astrocyte cultures exposed to HSF (P = 0.027), rTrCB1.1 (P < 0.001), and Recombinant T. regenti cathepsin B2 (rTrCB2) (P = 0.001), about 2.6-fold elevated levels of nitrite were detected if compared to the non-stimulated group
Summary
Helminth neuroinfections represent a serious health problem, but host immune mechanisms in the nervous tissue often remain undiscovered. Trichobilharzia regenti is widely distributed in Europe, e.g. Czech Republic [3], Denmark [4], France [5], Iceland [6] or Russia [7], and was detected in Iran [8] It uses anatid birds, e.g. ducks, as definitive hosts. Apart from birds, T. regenti cercariae are able to penetrate the skin of accidental mammalian hosts, e.g. mice or humans. This may result in a skin allergic reaction known as cercarial dermatitis which is regarded as a re-emerging disease [9,10,11]. To penetrate the host’s skin, cercariae are equipped with proteases present in their excretory/secretory products (ESP; [12]), such as cysteine protease cathepsin B2 from postacetabular glands that was shown to cleave skin proteins like collagen, keratin and elastin [13]
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