NDLI: Microglial cell response in α7 nicotinic acetylcholine receptor-deficient mice after systemic infection with Escherichia coli

Content Provider	Springer Nature : BioMed Central
Author	Hoogland, Inge C. M. Yik, Jutka Westhoff, Dunja Engelen-Lee, Joo-Yeon Valls Seron, Merche Man, Wing Kit Houben-Weerts, Judith H. P. M. Tanck, Michael W. T. van Westerloo, David J. van der Poll, Tom van Gool, Willem A. van de Beek, Diederik
Abstract	Background Development of neurodegeneration in older people has been associated with microglial cell activation triggered by systemic infection. We hypothesize that α7 nicotinic acetylcholine receptor (α7nAChR) plays an important role in regulation of this process. Methods 8- to 10-week-old male wild-type (WT) and α7nAChR knock-out (α7nAChR−/−) mice were intraperitoneally inoculated with live Escherichia (E.) coli or saline. After inoculation, all mice were treated with ceftriaxone (an antimicrobial drug) at 12 and 24 h and killed at 2 or 3 days. The microglial response was characterized by immunohistochemical staining with an ionized calcium-binding adaptor molecule 1 (Iba-1) antibody and flow cytometry. To quantify inflammatory response, mRNA expression of pro- and anti-inflammatory mediators was measured in brain and spleen. Results We observed no differences in Iba-1 positive cell number or morphology and flow cytometry (CD11b, CD45 and CD14) of microglial cells between WT and α7nAChR−/− mice after systemic infection. Infected α7nAChR−/− mice showed significantly higher mRNA expression in brain for tumor necrosis factor alpha (TNF-α) at day 2 and 3, interleukin 6 (IL-6) at day 2 and monocyte chemotactic protein 1 (MCP-1) and suppressor of cytokine signaling 1 (SOCS1) at day 3, there was significantly lower mRNA expression in brain for mitogen-activated protein kinase 1 (MAPK1) at day 2 and 3, high-mobility group 1 (HMGB-1) and CD11b at day 2, and deubiquitinase protein A20 (A20) at day 3 compared to infected WT mice. Interpretation Loss of function of α7nAChR during systemic infection led to an increased expression of TNF-α and IL-6 in brain after systemic infection with E. coli, but not to distinct differences in microglial cell number or morphological activation of microglia.
Related Links	https://jneuroinflammation.biomedcentral.com/counter/pdf/10.1186/s12974-022-02452-8.pdf
Ending Page	11
Page Count	11
Starting Page	1
File Format	HTM / HTML
ISSN	17422094
DOI	10.1186/s12974-022-02452-8
Journal	Journal of Neuroinflammation
Issue Number	1
Volume Number	19
Language	English
Publisher	BioMed Central
Publisher Date	2022-04-12
Access Restriction	Open
Subject Keyword	Neurosciences Neurology Neurobiology Immunology Escherichia coli Microglia Microglial activation Systemic infection Neuro-inflammation α7 acetylcholine receptor α7nAChR Knock-out Mouse model
Content Type	Text
Resource Type	Article
Subject	Neuroscience Immunology Cellular and Molecular Neuroscience Neurology
Journal Impact Factor	9.3/2023
5-Year Journal Impact Factor	9.8/2023

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