Altered expression of immune-related antigens by neuronophages does not improve neuronal survival after severe lesion of the facial nerve in rats

Angelov, Doychin N.; Krebs, Claudia; Walther, Michael; Martinez-Portillo, F.J.; Gunkel, A.; Lay, C.H.; Streppel, Michael; Guntinas‐Lichius, Orlando; Stennert, E.; Neiss, Wolfram F.

doi:10.1002/(sici)1098-1136(199810)24:2<155::aid-glia1>3.0.co;2-3

Cited by 14 publications

(8 citation statements)

References 83 publications

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“…In this context, the more prominent microglial response after nerve transection-resection may just be secondary to the more extensive neurodegeneration. Such an interpretation would be in line with previous observations of a correlation between the microglial response and neuron phagocytosis (72) and the extensive neuron loss and concomitant microglia response, including their transformation to cells positive for the phagocytosis marker ED1 following motor neuron axotomy in neonatal compared to adult animals (73).…”

Section: Role Of Microglia For Survival Of Axotomized Motor Neuronssupporting

confidence: 89%

Mechanisms and consequences of microglial responses to peripheral axotomy

Aldskogius¹

2011

Front Biosci

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Microglia respond rapidly to injury of peripheral nerve axons (axotomy). This response is integrated into the responses of the injured neurons, i.e. processes for neuron survival, axon regeneration and restoration of target contact. The microglial response is also integrated in changes in presynaptic terminals on axotomized motor or autonomic neurons and in changes in the central terminals of peripherally axotomized sensory neurons. Microglia also has an established role in interacting with astrocytes to shape their response to peripheral axotomy. Axotomy models in mice have demonstrated a role for microglia in regulating the entry of lymphocytes into motor nuclei or sensory areas following peripheral axotomy. Whether this is a universal component of peripheral nerve injury remains to be determined. Under certain circumstances, microglia activated by axotomy are major contributors to CNS pathology, e.g. in models of neuropathic pain. However, the general roles played by microglia after peripheral nerve injury are still incompletely understood. Early proposals that the microglial reaction to peripheral nerve injury is preparatory for the eventuality of neuron degeneration may still have relevance.

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Section: Role Of Microglia For Survival Of Axotomized Motor Neuronssupporting

confidence: 89%

Mechanisms and consequences of microglial responses to peripheral axotomy

Aldskogius¹

2011

Front Biosci

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“…Similarly, leptomeningeal macrophages but not microglia expressed CD163 (Figure 5B,C). Iba1 + pericytes expressed CD163 (Figure 5B, s blue arrowheads), as has been described elsewhere [23,26]. Thus, microglia in the brain parenchyma were CD68 − or weak, and CD163 − The isolated leptomeninges contained macrophages expressing CD68 and CD163 (Figure 5D,E).…”

Section: Resultssupporting

confidence: 75%

“…In fact, the ramified microglia in the neonatal rat brain parenchyma did not express CD68 or expressed it at quite a low level (Figure 5A), whereas macrophages in the leptomeninges strongly expressed it. Thus, ED1 is not suitable to identify ramified microglia in the normal brain parenchyma, as has been demonstrated elsewhere [23][24][25]. Similarly, leptomeningeal macrophages but not microglia expressed CD163 (Figure 5B,C).…”

Section: Resultsmentioning

confidence: 72%

Generation of CSF1-Independent Ramified Microglia-Like Cells from Leptomeninges In Vitro

Tanaka

Takahashi

Yano

et al. 2020

Cells

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Although del Río-Hortega originally reported that leptomeningeal cells are the source of ramified microglia in the developing brain, recent views do not seem to pay much attention to this notion. In this study, in vitro experiments were conducted to determine whether leptomeninges generate ramified microglia. The leptomeninges of neonatal rats containing Iba1+ macrophages were peeled off the brain surface. Leptomeningeal macrophages strongly expressed CD68 and CD163, but microglia in the brain parenchyma did not. Leptomeningeal macrophages expressed epidermal growth factor receptor (EGFR) as revealed by RT-PCR and immunohistochemical staining. Cells obtained from the peeled-off leptomeninges were cultured in a serum-free medium containing EGF, resulting in the formation of large cell aggregates in which many proliferating macrophages were present. In contrast, colony-stimulating factor 1 (CSF1) did not enhance the generation of Iba1+ cells from the leptomeningeal culture. The cell aggregates generated ramified Iba1+ cells in the presence of serum, which express CD68 and CD163 at much lower levels than primary microglia isolated from a mixed glial culture. Therefore, the leptomeningeal-derived cells resembled parenchymal microglia better than primary microglia. This study suggests that microglial progenitors expressing EGFR reside in the leptomeninges and that there is a population of microglia-like cells that grow independently of CSF1.

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“…Despite differences in FMN loss at 28 days, we were unable to show that these changes correlated with the magnitude of local inflammation in axotomized nuclei at 2 weeks post‐FNAx (compare Figs 2 and 3E and F). Others have also failed to establish a correlation between local inflammation and ensuing neurodegeneration after FNAx (Angelov et al. , 1998; Ha et al.…”

Section: Discussionmentioning

confidence: 99%

Central nervous system and non‐central nervous system antigen vaccines exacerbate neuropathology caused by nerve injury

Ankeny

Popovich

2007

Eur J of Neuroscience

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Previously, we showed that autoimmune (central nervous system myelin-reactive) T cells exacerbate tissue damage and impair neurological recovery after spinal cord injury. Conversely, independent studies have shown T cell-mediated neuroprotection after spinal cord injury or facial nerve axotomy (FNAx). The antigen specificity of the neuroprotective T cells has not been investigated after FNAx. Here, we compared the neuroprotective capacity of autoimmune and non-autoimmune lymphocytes after FNAx. Prior to axotomy, C57BL/6 mice were immunized with myelin basic protein, myelin oligodendrocyte glycoprotein (MOG) or ovalbumin (a non-self antigen) emulsified in complete Freund's adjuvant (CFA). FNAx mice receiving injections of phosphate-buffered saline (PBS) only (unimmunized) or PBS/CFA emulsions served as controls. At 4 weeks after axotomy, bilateral facial motor neuron counts were obtained throughout the facial motor nucleus using unbiased stereology (optical fractionator). The data show that neuroantigen immunizations and 'generic' lymphocyte activation (e.g. PBS/CFA or ovalbumin/CFA immunizations) exacerbated neuron loss above that caused by FNAx alone. We also found that nerve injury potentiated the effector potential of autoimmune lymphocytes. Indeed, prominent forelimb and hindlimb motor deficits were accompanied by disseminated neuroinflammation and demyelination in FNAx mice receiving subencephalitogenic immunization with MOG. FNAx or neuroantigen (MOG or myelin basic protein) immunization alone did not cause these pathological changes. Thus, irrespective of the antigens used to trigger an immune response, neuropathology was enhanced when the immune system was primed in parallel with nerve injury. These data have important implications for therapeutic vaccination in clinical neurotrauma and neurodegeneration.

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Altered expression of immune-related antigens by neuronophages does not improve neuronal survival after severe lesion of the facial nerve in rats

Cited by 14 publications

References 83 publications

Mechanisms and consequences of microglial responses to peripheral axotomy

Mechanisms and consequences of microglial responses to peripheral axotomy

Generation of CSF1-Independent Ramified Microglia-Like Cells from Leptomeninges In Vitro

Central nervous system and non‐central nervous system antigen vaccines exacerbate neuropathology caused by nerve injury

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