MicroRNA-155 knockout mice are susceptible to Mycobacterium tuberculosis infection. Issue 3 (May 2015)

• Record Type: Journal Article
• Authors: Iwai, Hiroki; Funatogawa, Keiji; Matsumura, Kazunori; Kato-Miyazawa, Masako; Kirikae, Fumiko; Kiga, Kotaro; Sasakawa, Chihiro; Miyoshi-Akiyama, Tohru; Kirikae, Teruo
• Is Part Of: Tuberculosis. Volume 95:Issue 3(2015)
• Page Start: 246
• Page End: 250
• Publication Date: 2015-05
• Subjects: 616.995
• DOI: 10.1016/j.tube.2015.03.006
• Languages: English
• ISSNs: 1472-9792

Abstract

<abstract xml:lang="en" abstract-type="author" id="abs0010"> <title id="sectitle0010">Summary</title> <sec> <p id="abspara0010">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 <italic>Mycobacterium tuberculosis</italic> 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 <italic>M. tuberculosis</italic>.</p> </sec> </abstract>