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Published on: July 3, 2025
MicroRNA-155 knockout mice are susceptible to Mycobacterium tuberculosis infection
Hiroki Iwai1, Keiji Funatogawa2, Kazunori Matsumura1
1Department of Infectious Diseases, Research Institute, National Center for Global Health and Medicine, Toyama, Shinjuku, Tokyo 162-8655, Japan.
Abstract:
MicroRNAs (miRNAs) are short, conserved, non-coding RNA molecules that repress translation, followed by the decay of miRNA-targeted mRNAs that encode molecules involved in cell differentiation, development, immunity and apoptosis. At least six miRNAs, including microRNA-155 (miR-155), were up-regulated when born marrow-derived macrophages from C57BL/6 mice were infected with Mycobacterium tuberculosis Erdman. C57BL/6 mice intravenously infected with Erdman showed up-regulation of miR-155 in livers and lungs. Following infection, miR-155-deficient C57BL/6 mice died significantly earlier and had significantly higher numbers of CFU in lungs than wild-type mice. Moreover, fewer CD4(+) T cells, but higher numbers of monocytes and neutrophils, were present in the lungs of Erdman-infected miR-155 knockout (miR-155(-/-)) than of wild-type mice. These findings indicated that miR-155 plays a critical role in immune responses to M. tuberculosis.
Insights
MicroRNA-155 (miR-155) is crucial for controlling Mycobacterium tuberculosis infection. Mice lacking miR-155 showed a weakened immune response and increased susceptibility to tuberculosis.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- MicroRNAs (miRNAs) are short, non-coding RNAs regulating gene expression.
- miRNAs are involved in critical cellular processes like immunity and apoptosis.
- Mycobacterium tuberculosis infection impacts host gene expression, including miRNAs.
Purpose of the Study:
- To investigate the role of microRNA-155 (miR-155) in the host immune response to Mycobacterium tuberculosis infection.
- To determine the impact of miR-155 deficiency on the course of tuberculosis in a mouse model.
Main Methods:
- Infection of bone marrow-derived macrophages and C57BL/6 mice with Mycobacterium tuberculosis Erdman strain.
- Quantification of miR-155 expression in infected tissues (livers, lungs).
- Comparison of disease progression, bacterial load (CFU), and immune cell infiltration in wild-type and miR-155 knockout mice.
Main Results:
- miR-155 was significantly upregulated in macrophages and tissues following M. tuberculosis infection.
- miR-155 deficient mice exhibited increased mortality and higher bacterial loads in the lungs.
- Absence of miR-155 led to altered immune cell populations in the lungs, with fewer CD4(+) T cells and more monocytes/neutrophils.
Conclusions:
- miR-155 plays a critical role in the immune defense against Mycobacterium tuberculosis.
- miR-155 is essential for regulating the appropriate immune cell response during tuberculosis infection.
- Targeting miR-155 pathways may offer novel therapeutic strategies for tuberculosis.
