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Published on: December 26, 2017
Inhibition of cell death of bone marrow-derived macrophages infected with Ehrlichia muris
Vivek Bhakta Mathema1, Zahid Manzoor, Jung-Eun Koo
1School of Medicine, Jeju National University, Jeju 690-756, South Korea.
Abstract:
Ehrlichia muris is a Gram-negative obligate intracellular bacterium belonging to the family Anaplasmataceae. It preferentially replicates inside macrophages by utilizing nutrients and processes of the host cell. In the present article, we studied the effects of E. muris infection on cell death of bone marrow-derived macrophages (BMDMs). Primary BMDMs were used for accessing E. muris-induced cell death, pro-inflammatory cytokine production and Western blot analysis. Human embryonic kidney cell line 293T (HEK293T) was used to access nuclear factor-kappaB (NF-κB) activity. BMDMs infected with E. muris showed significant inhibition of cell death when compared to uninfected cells. E. muris infection resulted in IκBα degradation, thus activation of NF-κB. In NF-κB reporter gene assay, the HEK293T cells infected with E. muris exhibited robust NF-κB-dependent luciferase activity in a bacterial dose-dependent manner. Furthermore, E. muris-induced inhibition of BMDMs cell death was abolished in the presence of MG132, a proteasome inhibitor that blocks NF-κB activation. Taken together, the results suggest that E. muris infection of BMDMs may have an inhibitory effect on cell death via a mechanism dependent on NF-κB activation.
Insights
Ehrlichia muris infection inhibits bone marrow-derived macrophage (BMDM) cell death by activating nuclear factor-kappaB (NF-κB). This protective effect is dependent on NF-κB activation, as shown by IκBα degradation and reporter gene assays.
Area of Science:
- Microbiology
- Immunology
- Cell Biology
Background:
- Ehrlichia muris is an obligate intracellular bacterium that infects macrophages.
- Macrophage apoptosis is crucial in host immune responses.
- Understanding pathogen-host interactions is vital for infectious disease research.
Purpose of the Study:
- To investigate the impact of Ehrlichia muris infection on macrophage cell death.
- To elucidate the role of nuclear factor-kappaB (NF-κB) signaling in E. muris-mediated effects on macrophages.
Main Methods:
- Bone marrow-derived macrophages (BMDMs) were infected with E. muris.
- Cell death was assessed, alongside pro-inflammatory cytokine production and Western blot analysis.
- NF-κB activity was measured using reporter gene assays in HEK293T cells and by analyzing IκBα degradation.
Main Results:
- E. muris infection significantly inhibited BMDM cell death compared to uninfected controls.
- E. muris infection led to IκBα degradation, indicating NF-κB activation.
- NF-κB-dependent luciferase activity was observed in infected HEK293T cells in a dose-dependent manner.
- The inhibition of cell death by E. muris was reversed by the proteasome inhibitor MG132.
Conclusions:
- Ehrlichia muris infection suppresses macrophage cell death.
- This suppression is mediated through the activation of the NF-κB signaling pathway.
- E. muris utilizes NF-κB activation as a mechanism to promote host cell survival during infection.
