Evaluation of miR-146a expression level in macrophages exposed to Candida glabrata

Authors

1 Department of Medical Parasitology and Mycology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

2 Department of Genetics and Molecular Biology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran

3 Department of Medical Genetics, School of Advanced Medical Technologies, Golestan University of Medical Sciences, Gorgan, Iran

4 Infectious Diseases and Tropical Medicine Research Center, Isfahan University of Medical Sciences, Isfahan, Iran

Abstract

Background and Purpose: MicroRNAs are small non-coding RNAs with 1924- nucleotides in length. Up- or downregulation
of many miRNAs has been shown by stimulation of Toll-like receptors (TLRs) in the innate immune system.
Up-regulation of miR-146a has been reported by both TLR and heat-killed Candida albicans. In this study, we aimed to
evaluate the expression of miR-146a in cultured monocyte-derived macrophages (MDMs) infected by Candida glabrata
at 12, 24, and 48 hours.
Materials and Methods: miR-146a expression was evaluated by qRT-real time polymerase chain reaction (PCR) at three
time points in C. glabrata-infected MDMs. The data was analyzed using repeated measures ANOVA.
Results: miR-146a expression was down-regulated in infected MDMs compared to the control group (p <0.018). The
expression of miR-146a was at its highest level at 48 h, as compared to 12 and 24 h (p <0.018). The differences between
the experimental group compared to the control group were statistically significant (p <0.018).
Conclusion: These results suggest that miR-146a can be involved in regulating macrophage function following TLR
stimulation in C. glabrata-infected MDMs.

Keywords

References

1. Pfaller MA, Messer SA, Moet GJ, Jones RN, Castanheira M. Candida bloodstream infections: comparison of species distribution and resistance to echinocandin and azole antifungal agents in Intensive Care Unit (ICU) and non-ICU settings in the SENTRY Antimicrobial Surveillance Program (2008–2009). Inter J Antimicrob Agen. 2011; 38(1):65-9.
2. Pfaller MA, Diekema DJ. Epidemiology of invasive candidiasis: a persistent public health problem. Clin Microbiol Rev. 2007; 20(1):133-63.
3. Ruan SY, Chu CC, Hsueh PR. In vitro susceptibilities of invasive isolates of Candida species: rapid increase in rates of fluconazole susceptible-dose dependent Candida glabrata isolates. Antimicrob Agents Chemother. 2008; 52(8):2919-22.
4. Fidel PL Jr, Vazquez JA, Sobel JD. Candida glabrata: review of epidemiology, pathogenesis, and clinical disease with comparison to C. albicans. Clin Microbiol Rev. 1999; 12(1):80-96.
5. Monk CE, Hutvagner G, Arthur JS. Regulation of miRNA transcription in macrophages in response to Candida albicans. PloS One. 2010; 5(10):e13669.
6. Denli AM, Tops BB, Plasterk RH, Ketting RF, Hannon GJ. Processing of primary microRNAs by the Microprocessor complex. Nature. 2004; 432(7014):231-5.
7. Gregory RI, Yan KP, Amuthan G, Chendrimada T, Doratotaj B, Cooch N, et al. The Microprocessor complex mediates the genesis of microRNAs. Nature. 2004; 432(7014):235-40.
8. Taganov KD, Boldin MP, Chang KJ, Baltimore D. NF-κB-dependent induction of microRNA miR- 146, an inhibitor targeted to signaling proteins of innate immune responses. Proc Natl Acad Sci U S A. 2006; 103(33):12481-6.
9. Reid DM, Gow NA, Brown GD. Pattern recognition: recent insights from Dectin-1. Curr Opin Immunol. 2009; 21(1):30-7.
10. Akira S, Uematsu S, Takeuchi O. Pathogen recognition and innate immunity. Cell. 2006; 124(4):783-801.
11. Takeuchi O, Akira S. Pattern recognition receptors and inflammation. Cell. 2010; 140(6):805-20.
12. Li Q, Verma IM. NF-κB regulation in the immune system. Nat Rev Immunol. 2002; 2(10):725-34.
13. Gilmore TD. Introduction to NF-κB: players, pathways, perspectives. Oncogene. 2006; 25(51):6680-4.
14. Hayden MS, Ghosh S. Shared principles in NF-κB signaling. Cell. 2008; 132(3):344-62.
15. Vaz C, Mer AS, Bhattacharya A, Ramaswamy R. MicroRNAs modulate the dynamics of the NF-κB signaling pathway. PloS One. 2011; 6(11):e27774.
16. Bartel DP. MicroRNAs: genomics, biogenesis, mechanism, and function. Cell. 2004; 116(2):281-97.
17. Bartel DP, Chen CZ. Micromanagers of gene expression: the potentially widespread influence of metazoan microRNAs. Nat Rev Genet. 2004; 5(5):396-400.
18. Lindsay MA. microRNAs and the immune response. Trends Immunol. 2008; 29(7):343-51.
19. Kasinski AL, Slack FJ. Potential microRNA therapies targeting Ras, NFκB and p53 signaling. Curr Opin Molecul Therap. 2010; 12(2):147-57.
20. Motsch N, Pfuhl T, Mrazek J, Barth S, Grässer FA. Epstein-Barr virus-encoded latent membrane protein 1 (LMP1) induces the expression of the cellular microRNA miR-146a. RNA Biol. 2007; 4(3):131-7.
21. Cameron JE, Yin Q, Fewell C, Lacey M, McBride J, Wang X, et al. Epstein-Barr virus latent membrane protein 1 induces cellular MicroRNA miR-146a, a modulator of lymphocyte signaling pathways. J Virol. 2008; 82(4):1946-58.
22. Seider K, Brunke S, Schild L, Jablonowski N, Wilson D, Majer O, et al. The facultative intracellular pathogen Candida glabrata subverts macrophage cytokine production and phagolysosome maturation. J Immunol. 2011; 187(6):3072-86.
Current Medical Mycology
Volume 2, Issue 2
June 2016
Pages 16-19

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