Differences in microglia activation between rats-derived cell and mice-derived cell after stimulating by soluble antigen of IV larva from Angiostrongylus cantonensis in vitro

Wei, Jie; Wu, Fengshi; Sun, Xi; Zeng, Xiaofeng; Liang, Jinyi; Zheng, Haixue; Yu, Xiaoli; Zhang, Kouxing; Wu, Zhongdao

doi:10.1007/s00436-012-3127-z

Cited by 23 publications

(7 citation statements)

References 22 publications

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“…However, histamine did not induce the release of TNF-α in the N9 microglia cell line [37], possibly because the microglia cell line is less sensitive than primary cultured microglia. In addition, the N9 microglia cell line is mouse-derived, and there are differences in microglial activation between rat-derived and mouse-derived cells [38]. In the present study, we also found that histamine was able to induce enhanced ROS production.…”

Section: Discussionsupporting

confidence: 73%

Activation of Microglia by Histamine and Substance P

Zhu

Lü

et al. 2014

Cell Physiol Biochem

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Background: Activated microglia perform many of the immune effector functions typically associated with macrophages. However, the regulators involved in microglial activation are not well defined. Because microglia play a pivotal role in immune surveillance of the CNS, we studied the effect of the neuromediators histamine and substance P on microglia. Methods: The induction of microglial activation by histamine and substance P was examined using primary cultured microglia. Fluorescent images were acquired with a confocal microscope. The levels of TNF-α and IL-6 were measured with a commercial ELISA kit. Intracellular reactive oxygen species (ROS) levels were determined by dichlorodihydrofluorescein oxidation. The mitochondrial membrane potential was assessed with the MitoProbe™ JC-1 assay kit. Results: We found that the neuromediators histamine and substance P were able to stimulate microglial activation and the subsequent production of ROS and proinflammatory factors TNF-α and IL-6. These effects were partially abolished by antagonists of the histamine receptors H1 and H4 and of the substance P receptors NK-1, NK-2 and NK-3. Histamine induced mitochondrial membrane depolarization in microglia. Conclusions: These results indicate that the neuromediators histamine and SP can trigger microglial activation and release of pro-inflammatory factors from microglia, thus contributing to the development of microglia-mediated inflammation in the brain.

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Section: Discussionsupporting

confidence: 73%

Activation of Microglia by Histamine and Substance P

Zhu

Lü

et al. 2014

Cell Physiol Biochem

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“…Contrary to LS, HSF triggered a significant production of NO in both astrocyte and microglia cultures. Similar effect (demonstrated at the level of enhanced iNOS expression) was shown for murine microglia treated in vitro with larval soluble antigen of the neurotropic nematode Angiostrongylus cantonensis [45]. As for T. regenti , NO production by glial cells might be associated with the in vivo occurring axonal damage [46, 47].…”

Section: Discussionmentioning

confidence: 60%

Nitric oxide and cytokine production by glial cells exposed in vitro to neuropathogenic schistosome Trichobilharzia regenti

et al. 2016

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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.

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“…RANTES (25) and eotaxin (26) are two important proinflammatory chemokines that are produced by T cells and antigenpresenting cells such as macrophages and microglia. RANTES, a 68-amino acid-long polypeptide, is known to induce the migration and homing of classical lymphoid cells such as T cells and monocytes and other immune cells including basophils, eosinophils, natural killer cells, dendritic cells, and mast cells (27).…”

Section: Discussionmentioning

confidence: 99%

Neutralization of RANTES and Eotaxin Prevents the Loss of Dopaminergic Neurons in a Mouse Model of Parkinson Disease

Chandra

Rangasamy

Roy

et al. 2016

Journal of Biological Chemistry

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Parkinson disease (PD) is second only to Alzheimer disease as the most common human neurodegenerative disorder. Despite intense investigation, no interdictive therapy is available for PD. Recent studies indicate that both innate and adaptive immune processes are active in PD. Accordingly, we found a rapid increase in RANTES (regulated on activation normal T cell expressed and secreted) and eotaxin, chemokines that are involved in T cell trafficking, in vivo in the substantia nigra pars compacta and the serum of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-intoxicated mice. RANTES and eotaxin were also up-regulated in the substantia nigra pars compacta of post-mortem PD brains as compared with age-matched controls. Therefore, we investigated whether neutralization of RANTES and eotaxin could protect against nigrostriatal degeneration in MPTP-intoxicated mice. Interestingly, after peripheral administration, functional blocking antibodies against RANTES and eotaxin reduced the infiltration of CD4(+) and CD8(+) T cells into the nigra, attenuated nigral expression of proinflammatory molecules, and suppressed nigral activation of glial cells. These findings paralleled dopaminergic neuronal protection, normalized striatal neurotransmitters, and improved motor functions in MPTP-intoxicated mice. Therefore, we conclude that attenuation of the chemokine-dependent adaptive immune response may be of therapeutic benefit for PD patients.

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Differences in microglia activation between rats-derived cell and mice-derived cell after stimulating by soluble antigen of IV larva from Angiostrongylus cantonensis in vitro

Cited by 23 publications

References 22 publications

Activation of Microglia by Histamine and Substance P

Activation of Microglia by Histamine and Substance P

Nitric oxide and cytokine production by glial cells exposed in vitro to neuropathogenic schistosome Trichobilharzia regenti

Neutralization of RANTES and Eotaxin Prevents the Loss of Dopaminergic Neurons in a Mouse Model of Parkinson Disease

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