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Updated: Jul 24, 2026
Three-dimensional Confocal Analysis of Microglia/macrophage Markers of Polarization in Experimental Brain Injury
Published on: September 4, 2013
Human microglia polarization following infection with the Lyme disease spirochete
Idris Akinlusi1, Brian Kan1, Ted Shi1
1Paul L. Foster School of Medicine, Texas Tech University Health Sciences Center, El Paso, TX, USA.
Abstract:
Infection with Borrelia burgdorferi can spread and cause central nervous system involvement, known as neuroborreliosis. Microglia phagocytose bacteria, mediate inflammation, and elicit an immune response toward the spirochete. Like other tissue macrophages, microglia can polarize into two different modulatory phenotypes, M1 and M2. We explored human microglial polarization changes upon infection with B. burgdorferi. HMC3 human microglia cell line was infected with B. burgdorferi for 24 h. Expression of polarization markers was evaluated via flow cytometry at 4 and 24 h. Secreted immunological mediators were evaluated using a multiplex ELISA system at 4, 18, and 24 h. An early decrease followed by a later increase in expression of M1 polarization marker iNOS was observed at 4 h, and 24 h, respectively. A decrease in M2 marker CX3CR1 occurred at 24 h. There were no changes in expression of M1 markers CD14, or in M2 markers CD163 and CD206. Multiplex ELISA evidenced an increase in secretion of activation markers MIP-1α, MIP- 1β, IP-10, chemotactic factor MCP-1, M1 polarization cytokine IL-8, and VEGF, at 4, 18, and 24 h. A decrease of iNOS at 4 h of infection suggests a diminished production of reactive nitrogen species that are a critical component of innate defense against infection. Increased iNOS and simultaneously decreased expression of CX3CR1 at 24 h, may suggest initiation of neuroprotective regulation of microglia recruitment to neuroinflammation. The dynamics of major inflammatory cytokines appear to be important in the microglial response to B. burgdorferi and should be further studied as these could become therapeutic targets in neuroborreliosis.
Insights
Neuroborreliosis involves central nervous system infection by Borrelia burgdorferi. This study shows microglia shift polarization markers and increase inflammatory mediators in response to B. burgdorferi infection.
Area of Science:
- Neuroimmunology
- Microbial Pathogenesis
Background:
- Borrelia burgdorferi infection can lead to neuroborreliosis, affecting the central nervous system.
- Microglia, the resident immune cells of the brain, play a crucial role in responding to pathogens like B. burgdorferi.
- Microglial cells exhibit polarization into M1 (pro-inflammatory) and M2 (anti-inflammatory/resolving) phenotypes, influencing the immune response.
Purpose of the Study:
- To investigate the dynamic changes in human microglial polarization upon infection with Borrelia burgdorferi.
- To identify key immunological mediators secreted by microglia during B. burgdorferi infection.
- To explore potential therapeutic targets for neuroborreliosis based on microglial responses.
Main Methods:
- Utilized the HMC3 human microglia cell line, infected with Borrelia burgdorferi.
- Evaluated the expression of M1 (iNOS, CD14) and M2 (CX3CR1, CD163, CD206) polarization markers using flow cytometry at 4 and 24 hours post-infection.
- Assessed the secretion of immunological mediators (MIP-1α, MIP-1β, IP-10, MCP-1, IL-8, VEGF) using multiplex ELISA at 4, 18, and 24 hours post-infection.
Main Results:
- Observed an early decrease followed by a late increase in inducible nitric oxide synthase (iNOS) expression (M1 marker).
- Noted a decrease in CX3CR1 expression (M2 marker) at 24 hours post-infection.
- Detected increased secretion of pro-inflammatory cytokines and chemokines, including MIP-1α, MIP-1β, IP-10, MCP-1, IL-8, and VEGF, at multiple time points.
Conclusions:
- Microglial response to Borrelia burgdorferi involves complex polarization dynamics, including an initial reduction and subsequent increase in iNOS.
- The observed changes in M1 and M2 markers suggest a shift towards a pro-inflammatory state, potentially impacting neuroinflammation.
- The elevated secretion of specific immunological mediators highlights their potential as therapeutic targets for managing neuroborreliosis.
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