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Neuroinflammation induced by intracerebroventricular injection of microbial neuraminidase.

Granados-Durán P, López-Ávalos MD, Grondona JM, Gómez-Roldán Mdel C, Cifuentes M, Pérez-Martín M, Alvarez M, Rodríguez de Fonseca F, Fernández-Llebrez P - Front Med (Lausanne) (2015)

Bottom Line: The expression of ICAM1 in the endothelial cells of the periventricular vessels, IBA1 in microglia, and GFAP in astrocytes notably increased in the regions reached by the injected neuraminidase.The subependymal microglia and the ventricular macrophages begun to express IL1β and some appeared to cross the ependymal layer.Thus, it is likely that a great part of the damage produced by microorganism invading the brain may be due to their neuraminidase content.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Biología Celular, Genética y Fisiología, Instituto de Investigación Biomédica de Málaga (IBIMA), Facultad de Ciencias, Universidad de Málaga , Málaga , Spain.

ABSTRACT
In the present paper, we describe the facts that took place in the rat brain after a single injection of the enzyme neuraminidase from Clostridium perfringens into the right lateral ventricle. After injection, it diffused through the cerebrospinal fluid of the ipsilateral ventricle and the third ventricle, and about 400 μm into the periventricular brain parenchyma. The expression of ICAM1 in the endothelial cells of the periventricular vessels, IBA1 in microglia, and GFAP in astrocytes notably increased in the regions reached by the injected neuraminidase. The subependymal microglia and the ventricular macrophages begun to express IL1β and some appeared to cross the ependymal layer. After about 4 h of the injection, leukocytes migrated from large venules of the affected choroid plexus, the meninges and the local subependyma, and infiltrated the brain. The invading cells arrived orderly: first neutrophils, then macrophage-monocytes, and last CD8α-positive T-lymphocytes and B-lymphocytes. Leukocytes in the ventricles and the perivascular zones penetrated the brain parenchyma passing through the ependyma and the glia limitans. Thus, it is likely that a great part of the damage produced by microorganism invading the brain may be due to their neuraminidase content.

No MeSH data available.


Related in: MedlinePlus

Lectin histochemistry in NA-injected rat brains immediately after the injection. (A,B) The site of injection is indicated with a red arrow in (A). Note a LFA-negative and PNA-positive halo around the injected lateral ventricle (i) and the third ventricle (IIIv) (double-headed arrow) but not the contralateral ventricle (cl). (C–F) Details of the zones squared in (A,B) showing the negative or positive halo (double-headed arrows). The squared areas are shown in detail in the following pictures. (G–J) The surface of the ependymal cells was LFA-negative (G) and PNA-positive (I) in the injected ventricle, whereas it was LFA-positive (H) and almost PNA-negative (J) in the contralateral ventricle. cc, corpus callosum; cl, contralateral ventricle; i, injected lateral ventricle; s, striatum; sf, septum-fimbria; IIIv, third ventricle. Sections in (A,C,D,G,H) were counterstained with hematoxilin–eosin.
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Figure 1: Lectin histochemistry in NA-injected rat brains immediately after the injection. (A,B) The site of injection is indicated with a red arrow in (A). Note a LFA-negative and PNA-positive halo around the injected lateral ventricle (i) and the third ventricle (IIIv) (double-headed arrow) but not the contralateral ventricle (cl). (C–F) Details of the zones squared in (A,B) showing the negative or positive halo (double-headed arrows). The squared areas are shown in detail in the following pictures. (G–J) The surface of the ependymal cells was LFA-negative (G) and PNA-positive (I) in the injected ventricle, whereas it was LFA-positive (H) and almost PNA-negative (J) in the contralateral ventricle. cc, corpus callosum; cl, contralateral ventricle; i, injected lateral ventricle; s, striatum; sf, septum-fimbria; IIIv, third ventricle. Sections in (A,C,D,G,H) were counterstained with hematoxilin–eosin.

Mentions: Animals were sacrificed immediately after the injection of NA (T: 0 h), LFA lectin exhibited a negative halo (~400 μm from the ventricle surface) around the injected lateral ventricle and the rostral third ventricle (Figures 1A,C). The ependymal surface of the injected lateral ventricle showed no staining at all (Figure 1G). Conversely, the contralateral ventricle showed no halo (Figures 1A,D) and a conspicuous staining of the subependyma and the surface of the ependymal cells (Figure 1H). On the contrary, when using PNA lectin (terminal galactose affinity) a positive label was found in the subependyma of the injected ventricle (Figures 1B,E) that was particularly intense in the surface of the ependymal cells (Figure 1I). The walls of the contralateral ventricle showed virtually no binding to PNA (Figures 1B,F), and the surface of the ependymal cells was only feebly positive (Figure 1J). After about a week, the ependymal cells that remained in the ventricular lining of the injected ventricle recovered the sialic acid and thus the LFA binding.


Neuroinflammation induced by intracerebroventricular injection of microbial neuraminidase.

Granados-Durán P, López-Ávalos MD, Grondona JM, Gómez-Roldán Mdel C, Cifuentes M, Pérez-Martín M, Alvarez M, Rodríguez de Fonseca F, Fernández-Llebrez P - Front Med (Lausanne) (2015)

Lectin histochemistry in NA-injected rat brains immediately after the injection. (A,B) The site of injection is indicated with a red arrow in (A). Note a LFA-negative and PNA-positive halo around the injected lateral ventricle (i) and the third ventricle (IIIv) (double-headed arrow) but not the contralateral ventricle (cl). (C–F) Details of the zones squared in (A,B) showing the negative or positive halo (double-headed arrows). The squared areas are shown in detail in the following pictures. (G–J) The surface of the ependymal cells was LFA-negative (G) and PNA-positive (I) in the injected ventricle, whereas it was LFA-positive (H) and almost PNA-negative (J) in the contralateral ventricle. cc, corpus callosum; cl, contralateral ventricle; i, injected lateral ventricle; s, striatum; sf, septum-fimbria; IIIv, third ventricle. Sections in (A,C,D,G,H) were counterstained with hematoxilin–eosin.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4362343&req=5

Figure 1: Lectin histochemistry in NA-injected rat brains immediately after the injection. (A,B) The site of injection is indicated with a red arrow in (A). Note a LFA-negative and PNA-positive halo around the injected lateral ventricle (i) and the third ventricle (IIIv) (double-headed arrow) but not the contralateral ventricle (cl). (C–F) Details of the zones squared in (A,B) showing the negative or positive halo (double-headed arrows). The squared areas are shown in detail in the following pictures. (G–J) The surface of the ependymal cells was LFA-negative (G) and PNA-positive (I) in the injected ventricle, whereas it was LFA-positive (H) and almost PNA-negative (J) in the contralateral ventricle. cc, corpus callosum; cl, contralateral ventricle; i, injected lateral ventricle; s, striatum; sf, septum-fimbria; IIIv, third ventricle. Sections in (A,C,D,G,H) were counterstained with hematoxilin–eosin.
Mentions: Animals were sacrificed immediately after the injection of NA (T: 0 h), LFA lectin exhibited a negative halo (~400 μm from the ventricle surface) around the injected lateral ventricle and the rostral third ventricle (Figures 1A,C). The ependymal surface of the injected lateral ventricle showed no staining at all (Figure 1G). Conversely, the contralateral ventricle showed no halo (Figures 1A,D) and a conspicuous staining of the subependyma and the surface of the ependymal cells (Figure 1H). On the contrary, when using PNA lectin (terminal galactose affinity) a positive label was found in the subependyma of the injected ventricle (Figures 1B,E) that was particularly intense in the surface of the ependymal cells (Figure 1I). The walls of the contralateral ventricle showed virtually no binding to PNA (Figures 1B,F), and the surface of the ependymal cells was only feebly positive (Figure 1J). After about a week, the ependymal cells that remained in the ventricular lining of the injected ventricle recovered the sialic acid and thus the LFA binding.

Bottom Line: The expression of ICAM1 in the endothelial cells of the periventricular vessels, IBA1 in microglia, and GFAP in astrocytes notably increased in the regions reached by the injected neuraminidase.The subependymal microglia and the ventricular macrophages begun to express IL1β and some appeared to cross the ependymal layer.Thus, it is likely that a great part of the damage produced by microorganism invading the brain may be due to their neuraminidase content.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Biología Celular, Genética y Fisiología, Instituto de Investigación Biomédica de Málaga (IBIMA), Facultad de Ciencias, Universidad de Málaga , Málaga , Spain.

ABSTRACT
In the present paper, we describe the facts that took place in the rat brain after a single injection of the enzyme neuraminidase from Clostridium perfringens into the right lateral ventricle. After injection, it diffused through the cerebrospinal fluid of the ipsilateral ventricle and the third ventricle, and about 400 μm into the periventricular brain parenchyma. The expression of ICAM1 in the endothelial cells of the periventricular vessels, IBA1 in microglia, and GFAP in astrocytes notably increased in the regions reached by the injected neuraminidase. The subependymal microglia and the ventricular macrophages begun to express IL1β and some appeared to cross the ependymal layer. After about 4 h of the injection, leukocytes migrated from large venules of the affected choroid plexus, the meninges and the local subependyma, and infiltrated the brain. The invading cells arrived orderly: first neutrophils, then macrophage-monocytes, and last CD8α-positive T-lymphocytes and B-lymphocytes. Leukocytes in the ventricles and the perivascular zones penetrated the brain parenchyma passing through the ependyma and the glia limitans. Thus, it is likely that a great part of the damage produced by microorganism invading the brain may be due to their neuraminidase content.

No MeSH data available.


Related in: MedlinePlus