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Spatial analysis of microglial and vascular responses following recurrent intranasal Group A Streptococcus infections

ABSTRACT: Spatial analysis of microglial and vascular responses following recurrent intranasal Group A Streptococcus infections

PROVIDER: PRJNA912763 | ENA |

REPOSITORIES: ENA

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Spatial analysis of microglial and vascular responses following recurrent intranasal Group A Streptococcus infections

Project description:Peripheral infections can result in neurocognitive changes in many contexts, including after recurrent Group A Streptococcus (GAS) infections in children. To explore the underlying mechanisms, here we used an intranasal inoculation model to analyze nearly 200,000 cells from the mouse olfactory bulb (OB) by multiplexed error-robust fluorescent in situ hybridization (MERFISH). Upon repeated GAS inoculations, endothelial cells (ECs) responded by downregulating blood-brain barrier and extracellular matrix genes. Microglia upregulated response to interferon and antigen presentation genes and downregulated homeostatic microglia genes. We determined that microglia with higher expression of Streptococcus-responsive genes were localized to the outer glomerular layer of the OB, possibly due to their proximity to infiltrating CD4 T cells. Expression of homeostatic genes was correspondingly high in the inner granular layer of the OB.

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Effects of Th17 cytokines on microglial responses and the blood-brain barrier following recurrent intranasal Group A Streptococcus infections

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Effects of Th17 cytokines on microglial responses and the blood-brain barrier following recurrent intranasal Group A Streptococcus infections

Project description:Effects of Th17 cytokines on microglial responses and the blood-brain barrier following recurrent intranasal Group A Streptococcus infections

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Effects of Th17 cytokines on transcriptome of primary microglial cultures in vitro

Project description:Peripheral infections can result in neuropsychiatric changes in many contexts, including after recurrent Group A Streptococcus (GAS) infections in children. In a mouse model of intranasal GAS inoculation, we have previously demonstrated in vivo that mice lacking Th17 cells, or the key Th17 cytokines interleukin 17A (IL-17A) or granulocyte-macrophage colony-stimulating factor (GM-CSF), have altered microglial responses. As an attempt to determine whether these cytokines have direct effects on microglia, we cultured primary microglia and incubated them with either interferon gamma (IFNg), IL-17A or GM-CSF for 24 hours, then collected RNA for bulk sequencing. Microglia treated with IFNg or GM-CSF displayed striking transcriptional shifts, including upregulation of many inflammatory genes. IL-17A treatment did not have a noticeable effect on the microglial transcriptome, likely due to the in vitro absence of IL-17A receptors, which are expressed by microglia in vivo.

2023-03-14 | GSE221715 | GEO

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