Differential migration, LPS‐induced cytokine, chemokine, and NO expression in immortalized BV‐2 and HAPI cell lines and primary microglial cultures
Open accessAbstract
Microglial cells are hematopoietically derived monocytes of the CNS and serve important neuromodulatory, neurotrophic, and neuroimmune roles. Following insult to the CNS, microglia develop a reactive phenotype, migrate to the site of injury, proliferate, and release a range of proinflammatory, anti‐inflammatory, and neurotrophic factors. Isolation of primary microglial cell cultures has been an integral step in elucidating the many roles of these cells. In addition to primary microglial cells, several immortalized cell lines have been created to model primary microglia in vitro, including murine‐derived BV‐2 cells and rat derived highly aggressive proliferating immortalized (HAPI) cells. Here, we compare rat primary microglial, BV‐2, and HAPI cells in experiments assessing migration, expression of activation markers, and production and release of nitric oxide, cytokines, and chemokines. BV‐2 and HAPI cells responded similarly to primary microglia in experiments assessing migration, ionized calcium binding adaptor molecule 1 expression, and nitric oxide release. However, BV‐2 and HAPI cells did not model primary microglia in experiments assessing tumor necrosis factor‐α, interleukin‐1β, interleukin‐6, and monocyte chemoattractant protein‐1 expression and release and phospho‐extracellular signal‐regulated kinase 44/42 expression following lipopolysaccharide treatment. These results indicate that BV‐2 and HAPI cell cultures only partially model primary microglia and that their use should therefore be carefully considered.
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Differences between immortalized cell lines and primary murine microglia are not insignificant.
“However, several reports have indicated that differences between immortalized cell lines and primary murine microglia are not insignificant [83,84].”
From Lipoprotein Lipase Regulates Microglial Lipid Droplet Accumulation (2021) · cites this paper as [83]
The Discussion reports substantial differences between the immortalized BV-2 and HAPI lines and primary microglia, particularly in inflammatory responses. However, the Abstract specifies that the primary cultures tested were rat, not murine; the source therefore does not directly establish the claim for primary murine microglia. Page numbers were not provided in our copy. (LLM, conf=0.86)
Experimental — accuracy not yet measuredBV-2 cells show damped cytokine release compared to primary microglia, while responding similarly in migration and activation experiments.
“In particular, while BV-2 and primary microglia respond similarly in migration and activation experiments, BV-2 cells show a damped cytokine release [83].”
From Lipoprotein Lipase Regulates Microglial Lipid Droplet Accumulation (2021) · cites this paper as [83]
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“In particular, while BV-2 and primary microglia respond similarly in migration and activation experiments, BV-2 cells show a damped cytokine release [83].”
BackgroundBenfotiamine Attenuates Inflammatory Response in LPS Stimulated BV-2 Microglia
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- Authors
- Horvath, R. J., Nutile‐McMenemy, N., Alkaitis, M. S., & DeLeo, J. A.
- Affiliations
- Dartmouth College (US)
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2008-10
- Volume
- 107
- Issue
- 2
- Pages
- 557-569
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- PMC
- PMC2581646
- OpenAlex
- W1509256585
- Cited by
- 264
- References
- 1
- Citations by year
- 2026: 8 · 2025: 10 · 2024: 13 · 2023: 11 · 2022: 25 · 2021: 24 · 2020: 16 · 2019: 11 · 2018: 21 · 2017: 13 · 2016: 11 · 2015: 17 · 2014: 12 · 2013: 17 · 2012: 17
- FWCI
- 8.14
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute on Drug Abuse (DA 11276, R01DA011276)
- National Institute of Allergy and Infectious Diseases (T32AI07363, T32AI007363)
- National Institute of Arthritis and Musculoskeletal and Skin Diseases (AR44757, R01AR044757)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- microglia, BV-2 cells, microglial migration, lipopolysaccharide, neuroinflammation, nitric oxide, cytokines, chemokines, TNF-α, IL-1β, interleukin-6, MCP-1, ERK1/2 phosphorylation, Iba1
- MeSH terms
- Animals, Animals, Newborn, Calcium-Binding Proteins, Cell Movement, Cells, Cultured, Cerebral Cortex, Dose-Response Relationship, Drug, Enzyme-Linked Immunosorbent Assay, Lipopolysaccharides, Microfilament Proteins, Minocycline, Nitric Oxide, Time Factors, Xanthines, Cytokines, Microglia, Neuroprotective Agents, Extracellular Signal-Regulated MAP Kinases, Mice, Rats
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