engleski

Murine cytomegalovirus as a cellular re-engineer of BV-2 microglial cells

Microglial cells are the residential phagocytic cells in the brain, originating from the same progenitors as peripheral macrophages. They perform various macrophage-like functions like phagocytosis, antigen presentation and damages tissue repair. They possess several activation states, depending on various stimuli, from a ramified, resting shape in a healthy brain to a more condensed, activated form in a brain exposed to endogenous or exogenous stimuli. Homeostasis disruption leads to the adaptation of morphology and function, suited to the causal stimuli. It has widely been established that they separate themselves into M1 and M2 phenotypes depending on these stimuli, however further studies point out even more types that are still being characterized. The aim of our study is to determine how the murine cytomegalovirus (MCMV) infection affects the microglia in both form and function. Our in-vitro studies are based on the BV-2 microglial immortalized culture. We used the method of immunofluorescence and light microscopy to observe the effects of MCMV on the cell line. Markers used were Arginase-1 and CD206 for M2, while iNOS and CD16/32 measured M1 activity. HIF-1alpha was used as a marker of metabolic activity. The cells were analyzed after 24h and 48h of infection. Infected cells changed their morphology from ramified to ameboid. Likewise, infected cells had a higher expression of M1 markers over M2, measured by immunofluorescence. There were no significant differences in both times of infection. Our results indicate that the MCMV modified both the morphology and phenotype of microglial cells, causing them to subtly shift to a M1, pathogen killing, phenotype.

microglia cells, cytomegalovirus, immunometabolomics

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