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Sympathetic glial cells and macrophages develop different responses to Trypanosoma cruzi infection or lipopolysaccharide stimulation.

de Almeida-Leite CM, Silva IC, Galvão LM, Arantes RM - Mem. Inst. Oswaldo Cruz (2014)

Bottom Line: T. cruzi infection was greater in glial cells, despite similar levels of NO production in both cell types.Glial cells responded similarly to T. cruzi and LPS, but were less responsive to LPS than macrophages were.Moreover, our findings will facilitate future research into the immune responses and activation mechanisms of peripheral glial cells, which are important for understanding the paradoxical responses of this cell type in neuronal lesions and neuroprotection.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brasil.

ABSTRACT
Nitric oxide (NO) participates in neuronal lesions in the digestive form of Chagas disease and the proximity of parasitised glial cells and neurons in damaged myenteric ganglia is a frequent finding. Glial cells have crucial roles in many neuropathological situations and are potential sources of NO. Here, we investigate peripheral glial cell response to Trypanosoma cruzi infection to clarify the role of these cells in the neuronal lesion pathogenesis of Chagas disease. We used primary glial cell cultures from superior cervical ganglion to investigate cell activation and NO production after T. cruzi infection or lipopolysaccharide (LPS) exposure in comparison to peritoneal macrophages. T. cruzi infection was greater in glial cells, despite similar levels of NO production in both cell types. Glial cells responded similarly to T. cruzi and LPS, but were less responsive to LPS than macrophages were. Our observations contribute to the understanding of Chagas disease pathogenesis, as based on the high susceptibility of autonomic glial cells to T. cruzi infection with subsequent NO production. Moreover, our findings will facilitate future research into the immune responses and activation mechanisms of peripheral glial cells, which are important for understanding the paradoxical responses of this cell type in neuronal lesions and neuroprotection.

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: Trypanosoma cruzi infection and inducible nitric oxidesynthase (iNOS) expression in glial cells and macrophages. A: percentage ofT. cruzi-infected cells in glial cell or macrophagecultures. The data correspond to the mean of five independent experiments ±standard error of the mean (SEM). Asterisks mean statistically significantdifference (p < 0.01, unpaired t test); B: number ofamastigotes/cell in T. cruzi-infected glial cell or macrophagecultures. The data correspond to the mean of five independent experiments ± SEM(p < 0.05, unpaired t test); C: intensity of iNOSimmunofluorescence in T. cruzi-infected glial cell ormacrophage cultures 48 h post-intervention. The data correspond to the mean oftwo independent experiments in triplicate ± SEM (p < 0.05, unpairedt test); A: aminoguainidine; G: glial cell; I:interferon-γ; M: macrophage; T: T. cruzi.
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f02: : Trypanosoma cruzi infection and inducible nitric oxidesynthase (iNOS) expression in glial cells and macrophages. A: percentage ofT. cruzi-infected cells in glial cell or macrophagecultures. The data correspond to the mean of five independent experiments ±standard error of the mean (SEM). Asterisks mean statistically significantdifference (p < 0.01, unpaired t test); B: number ofamastigotes/cell in T. cruzi-infected glial cell or macrophagecultures. The data correspond to the mean of five independent experiments ± SEM(p < 0.05, unpaired t test); C: intensity of iNOSimmunofluorescence in T. cruzi-infected glial cell ormacrophage cultures 48 h post-intervention. The data correspond to the mean oftwo independent experiments in triplicate ± SEM (p < 0.05, unpairedt test); A: aminoguainidine; G: glial cell; I:interferon-γ; M: macrophage; T: T. cruzi.

Mentions: To determine the infection rate, parasitised cells in both cultures were counted. Aquantitative analysis showed a higher number of infected cells in the glial cellcultures than in the macrophage cultures (Fig.2A). However, when iNOS activity was blocked by AG, there was a significantdecrease in the number of infected glial cells, with a significant increase in infectedmacrophages (Fig. 2A).


Sympathetic glial cells and macrophages develop different responses to Trypanosoma cruzi infection or lipopolysaccharide stimulation.

de Almeida-Leite CM, Silva IC, Galvão LM, Arantes RM - Mem. Inst. Oswaldo Cruz (2014)

: Trypanosoma cruzi infection and inducible nitric oxidesynthase (iNOS) expression in glial cells and macrophages. A: percentage ofT. cruzi-infected cells in glial cell or macrophagecultures. The data correspond to the mean of five independent experiments ±standard error of the mean (SEM). Asterisks mean statistically significantdifference (p < 0.01, unpaired t test); B: number ofamastigotes/cell in T. cruzi-infected glial cell or macrophagecultures. The data correspond to the mean of five independent experiments ± SEM(p < 0.05, unpaired t test); C: intensity of iNOSimmunofluorescence in T. cruzi-infected glial cell ormacrophage cultures 48 h post-intervention. The data correspond to the mean oftwo independent experiments in triplicate ± SEM (p < 0.05, unpairedt test); A: aminoguainidine; G: glial cell; I:interferon-γ; M: macrophage; T: T. cruzi.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4155848&req=5

f02: : Trypanosoma cruzi infection and inducible nitric oxidesynthase (iNOS) expression in glial cells and macrophages. A: percentage ofT. cruzi-infected cells in glial cell or macrophagecultures. The data correspond to the mean of five independent experiments ±standard error of the mean (SEM). Asterisks mean statistically significantdifference (p < 0.01, unpaired t test); B: number ofamastigotes/cell in T. cruzi-infected glial cell or macrophagecultures. The data correspond to the mean of five independent experiments ± SEM(p < 0.05, unpaired t test); C: intensity of iNOSimmunofluorescence in T. cruzi-infected glial cell ormacrophage cultures 48 h post-intervention. The data correspond to the mean oftwo independent experiments in triplicate ± SEM (p < 0.05, unpairedt test); A: aminoguainidine; G: glial cell; I:interferon-γ; M: macrophage; T: T. cruzi.
Mentions: To determine the infection rate, parasitised cells in both cultures were counted. Aquantitative analysis showed a higher number of infected cells in the glial cellcultures than in the macrophage cultures (Fig.2A). However, when iNOS activity was blocked by AG, there was a significantdecrease in the number of infected glial cells, with a significant increase in infectedmacrophages (Fig. 2A).

Bottom Line: T. cruzi infection was greater in glial cells, despite similar levels of NO production in both cell types.Glial cells responded similarly to T. cruzi and LPS, but were less responsive to LPS than macrophages were.Moreover, our findings will facilitate future research into the immune responses and activation mechanisms of peripheral glial cells, which are important for understanding the paradoxical responses of this cell type in neuronal lesions and neuroprotection.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Morfologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brasil.

ABSTRACT
Nitric oxide (NO) participates in neuronal lesions in the digestive form of Chagas disease and the proximity of parasitised glial cells and neurons in damaged myenteric ganglia is a frequent finding. Glial cells have crucial roles in many neuropathological situations and are potential sources of NO. Here, we investigate peripheral glial cell response to Trypanosoma cruzi infection to clarify the role of these cells in the neuronal lesion pathogenesis of Chagas disease. We used primary glial cell cultures from superior cervical ganglion to investigate cell activation and NO production after T. cruzi infection or lipopolysaccharide (LPS) exposure in comparison to peritoneal macrophages. T. cruzi infection was greater in glial cells, despite similar levels of NO production in both cell types. Glial cells responded similarly to T. cruzi and LPS, but were less responsive to LPS than macrophages were. Our observations contribute to the understanding of Chagas disease pathogenesis, as based on the high susceptibility of autonomic glial cells to T. cruzi infection with subsequent NO production. Moreover, our findings will facilitate future research into the immune responses and activation mechanisms of peripheral glial cells, which are important for understanding the paradoxical responses of this cell type in neuronal lesions and neuroprotection.

Show MeSH
Related in: MedlinePlus