An ex vivo ruminal ovine model to study the immediate immune response in the context of bacterial lipopolysaccharide

Abouhajer, Fathi; El‐Ashram, Saeed; Karama, Musafiri; Huang, Shujian; Liu, Jianfeng

doi:10.1007/s10142-018-0589-9

Cited by 5 publications

(2 citation statements)

References 47 publications

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“…Total RNA was extracted from astrocytes using Trizol reagent (Tiangen Biotech, China) according to the manufacturer's protocols. The concentrations of the extracted RNA were measured using NanoDrop 2000c (ThermoFisher, USA) (23–25). Total RNA (1 μg) was reverse-transcribed to cDNA using a reverse transcription kit (TaKaRa, Japan).…”

Section: Methodsmentioning

confidence: 99%

The Neurotropic Parasite Toxoplasma gondii Induces Astrocyte Polarization Through NFκB Pathway

et al. 2019

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Background: Toxoplasma gondii is a protozoan parasite that chronically infects nearly one-third of the world's human population. In immunosuppressed individuals and fetus, infection with T. gondii contributes to a series of devastating conditions, including toxoplasmic encephalitis (TE), which is characterized by neuron damage in the central nervous system (CNS). Astrocyte polarization is currently found in some neurodegenerative diseases, and A1 subtype of astrocyte leads to neuron apoptosis. However, little information has been available on the role of astrocyte polarization in TE.Methods: In the present study, we established a mouse model to study TE and detected A1 astrocyte in the brains of mice with TE. Expression level of A1 astrocyte-specific marker C3 was evaluated using indirect fluorescent assay (IFA) and Western blotting. Primary mouse astrocytes were incubated with different concentrations of T. gondii excreted-secreted antigens (TgESAs) in vitro. Expression level of C3 and A1 astrocyte-specific transcription levels were assessed using Western blotting and qRT-PCR, respectively. Bay11-7082 was used to study nuclear factor (NF) κB pathway in TgESA-induced astrocyte polarization.Results: In mice with TE, the proportion of A1 astrocyte (GFAP+C3+) increased significantly. The results of in vitro study showed that TgESAs induced astrocyte polarization to A1 subtype. Blocking of NFκB pathway by Bay11-7082 inhibited TgESA-induced astrocyte polarization.Conclusions: Our preliminary study showed the involvement of A1 astrocyte in the process of TE in mice, and TgESAs could trigger astrocyte to polarize to A1 subtype. These findings suggest a new mechanism underlying the neuropathogenesis induced by T. gondii infection.

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Section: Methodsmentioning

confidence: 99%

The Neurotropic Parasite Toxoplasma gondii Induces Astrocyte Polarization Through NFκB Pathway

et al. 2019

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“…The integrity of the isolated RNA was not evaluated in our experiments. The concentration of the extracted RNA was quantified using a NanoDrop 2000c spectrophotometer (ThermoFisher, USA) 27 – 29 . One microgram of the total RNA was then reverse-transcribed into cDNA using a reverse transcription kit from TaKaRa (Japan,Cat# 639,505).…”

Section: Methodsmentioning

confidence: 99%

Observing astrocyte polarization in brains from mouse chronically infected with Toxoplasma gondii

Yao,

Yuan,

Sheng

et al. 2024

Sci Rep

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Toxoplasma gondii (T. gondii) is a protozoan parasite that infects approximately one-third of the global human population, often leading to chronic infection. While acute T. gondii infection can cause neural damage in the central nervous system and result in toxoplasmic encephalitis, the consequences of T. gondii chronic infection (TCI) are generally asymptomatic. However, emerging evidence suggests that TCI may be linked to behavioral changes or mental disorders in hosts. Astrocyte polarization, particularly the A1 subtype associated with neuronal apoptosis, has been identified in various neurodegenerative diseases. Nevertheless, the role of astrocyte polarization in TCI still needs to be better understood. This study aimed to establish a mouse model of chronic TCI and examine the transcription and expression levels of glial fibrillary acidic protein (GFAP), C3, C1q, IL-1α, and TNF-α in the brain tissues of the mice. Quantitative real-time PCR (qRT-PCR), enzyme-linked immunosorbent assay, and Western blotting were employed to assess these levels. Additionally, the expression level of the A1 astrocyte-specific marker C3 was evaluated using indirect fluorescent assay (IFA). In mice with TCI, the transcriptional and expression levels of the inflammatory factors C1q, IL-1α, and TNF-α followed an up-down-up pattern, although they remained elevated compared to the control group. These findings suggest a potential association between astrocyte polarization towards the A1 subtype and synchronized changes in these three inflammatory mediators. Furthermore, immunofluorescence assay (IFA) revealed a significant increase in the A1 astrocytes (GFAP+C3+) proportion in TCI mice. This study provides evidence that TCI can induce astrocyte polarization, a biological process that may be influenced by changes in the levels of three inflammatory factors: C1q, IL-1α, and TNF-α. Additionally, the release of neurotoxic substances by A1 astrocytes may be associated with the development of TCI.

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Oral inoculation of ultraviolet-irradiated Eimeria species oocysts protects chickens against coccidiosis

et al. 2019

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An ex vivo ruminal ovine model to study the immediate immune response in the context of bacterial lipopolysaccharide

Cited by 5 publications

References 47 publications

The Neurotropic Parasite Toxoplasma gondii Induces Astrocyte Polarization Through NFκB Pathway

The Neurotropic Parasite Toxoplasma gondii Induces Astrocyte Polarization Through NFκB Pathway

Observing astrocyte polarization in brains from mouse chronically infected with Toxoplasma gondii

Oral inoculation of ultraviolet-irradiated Eimeria species oocysts protects chickens against coccidiosis

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