Abstract Views
PDF Download

The effects of Candida albicans and Candida krusei on expression of toll-like receptors and chemokine receptors by dendritic cells


Resistance to candidiasis requires the coordinated action of innate and adaptive immunity. Dendritic cells (DCs) are the most crucial antigen presenting cells and playing important role in initiation of innate and adaptive immunity. The aim of this study is to investigate the effects of the different concentrations of C. albicans (Candida albicans) and C. krusei on expression of TLR2, TLR4, TLR6, CCR5, CXCR4 and CX3CR1 in in-vitro dendritic cell (DC) cultures.

There were twelve experimental models for each C. albicans and C. krusei strains. The six of them contained monocyte derived dendritic cells with a concentration of 2x106 cells/ml, six of them did not. While two control models did not contain yeast cells, the others contained yeast cells with the concentrations of 1x106 cells/ml, 2x106 cells/ml, 4x106 cells/ml, 8x106 cells/ml 10x106 cells/ml, respectively. Two sets of these culture plates were incubated at 35°C with 5% CO2, one set for 24 hours and one set for 48 hours. At the end of the incubation periods, TLR2, TLR4, TLR6, CCR5, CXCR4 and CX3CR1 expression levels were analyzed with ELISA.

There were distinct increases in TLR2, TLR4, TLR6, CCR5 and CXCR4 expression levels as C. albicans strain concentration increases in experiment models which included DCs. On the other hand, there were apparent increases in TLR2, TLR4, CCR5 and CXCR4 expression levels as C. krusei strain concentration increases in experiment models which include DCs. But there was no explicit difference between TLRs and chemokine receptor expression levels and C. albicans and C. krusei strain concentrations in experiment models without DCs.

The activation of DCs leads to the release of several inflammatory mediators such as TLRs and chemokines. TLRs and chemokines take a role in early phase of infection, TLRs take part in recognition and producing a signal, and chemokines take part a role in transmitting this signal to the effector cells.

There is no Figure or data content available for this article


  • References
  • Yáñez, A., Megías, J., O'Connor, J.E., Gozalbo, D., Gil, M.L. 2011. Candida albicans induces selective development of macrophages and monocyte derived dendritic cells by a TLR2 dependent signalling. PLoS One 6, e24761.
  • Bahri, R., Saidane-Mosbahi, D., Rouabhia, M. 2010. Candida famata modulates toll-like receptor, beta-defensin, and proinflammatory cytokine expression by normal human epithelial cells. J Cell Physiol 222, 209.
  • Bustamante, C.I. 2005. Treatment of Candida infection: a view from the trenches! Curr Opin Infect Dis 18, 490.
  • Sobel, J.D. 2006. The emergence of non-albicans Candida species as causes of invasive candidiasis and candidemia. Curr Infect Dis Rep 8, 427.
  • Romani, L. 2011. Immunity to fungal infections. Nat Rev Immunol 11, 275.
  • Hohl, T.M., Rivera, A., Pamer, E.G. 2006. Immunity to fungi. Curr Opin Immunol 18, 465.
  • Re, F., Strominger, J.L. 2004. Heterogeneity of TLR-induced responses in dendritic cells: from innate to adaptive immunity. Immunobiology 209, 191.
  • Agrawal, A., Agrawal, S., Gupta, S. 2007. Dendritic cells in human aging. Exp Gerontol 42, 421.
  • You, J., Dong, H., Mann, E.R., Knight, S.C., Yaqoob, P. 2013. Ageing impairs the T cell response to dendritic cells. Immunobiology 218, 1077.
  • Liu, J., Geng, F., Sun, H., Wang, X., Zhang, H., Yang, Q., Zhang, J. 2018. Candida albicans induces TLR2/MyD88/NF-?B signaling and inflammation in oral lichen planus-derived keratinocytes. J Infect Dev Ctries 12, 780.
  • Kawai, T., Akira, S. 2010. The role of pattern-recognition receptors in innate immunity: update on Toll-like receptors. Nat Immunol 11, 373.
  • Yuan, X., Wilhelmus, K.R. 2010. Toll-like receptors involved in the pathogenesis of experimental Candida albicans keratitis. Invest Ophthalmol Vis Sci 51, 2094.
  • Jouault, T., Sarazin, A., Martinez-Esparza, M., Fradin, C., Sendid, B., Poulain, D. 2009. Host responses to a versatile commensal: PAMPs and PRRs interplay leading to tolerance or infection by Candida albicans. Cell Microbiol 11, 1007.
  • Gil, M.L., Gozalbo, D. 2009. Role of Toll-like receptors in systemic Candida albicans infections. Front Biosci (Landmark Ed) 14, 570.
  • Nagai, Y., Garrett, K.P., Ohta, S., Bahrun, U., Kouro, T., Akira, S., Takatsu, K., Kincade, P.W. 2006. Toll-like receptors on hematopoietic progenitor cells stimulate innate immune system replenishment. Immunity 24, 801.
  • Yáñez, A., Murciano, C., O'Connor, J.E., Gozalbo, D., Gil, M.L. 2009. Candida albicans triggers proliferation and differentiation of hematopoietic stem and progenitor cells by a MyD88-dependent signaling. Microbes Infect 11, 531.
  • Downes, J.E., Marshall-Clarke, S. 2010. Innate immune stimuli modulate bone marrow-derived dendritic cell production in vitro by toll-like receptor-dependent and -independent mechanisms. Immunology 131, 513.
  • Swidergall, M. 2019. Candida albicans at Host Barrier Sites: Pattern Recognition Receptors and Beyond. Pathogens (Basel, Switzerland) 8, 40.
  • Netea, M.G., van de Veerdonk, F., Verschueren, I., van der Meer, J.W., Kullberg, B.J. 2008. Role of TLR1 and TLR6 in the host defense against disseminated candidiasis. FEMS Immunol Med Microbiol 52, 118.
  • Bellocchio, S., Moretti, S., Perruccio, K., Fallarino, F., Bozza, S., Montagnoli, C., Mosci, P., Lipford, G.B., Pitzurra, L., Romani, L. 2004. TLRs govern neutrophil activity in aspergillosis. J Immunol 173, 7406.
  • Gafa, V., Remoli, M.E., Giacomini, E., Gagliardi, M.C., Lande, R., Severa, M., Grillot, R., Coccia, E.M. 2007. In vitro infection of human dendritic cells by Aspergillus fumigatus conidia triggers the secretion of chemokines for neutrophil and Th1 lymphocyte recruitment. Microbes Infect 9, 971.
  • Hong, M., Ryan, K.R., Arkwright, P.D., Gennery, A.R., Costigan, C., Dominguez, M., Denning, D.W., McConnell, V., Cant, A.J., Abinun, M., Spickett, G.P., Swan, D.C., Gillespie, C.S., Young, D.A., Lilic, D. 2009. Pattern recognition receptor expression is not impaired in patients with chronic mucocutanous candidiasis with or without autoimmune polyendocrinopathy candidiasis ectodermal dystrophy. Clin Exp Immunol 156, 40.
  • Megías, J., Maneu, V., Salvador, P., Gozalbo, D., Gil, M.L. 2013. Candida albicans stimulates in vivo differentiation of haematopoietic stem and progenitor cells towards macrophages by a TLR2-dependent signalling. Cell Microbiol 15, 1143.
  • do Nascimento, M.P., Pinke, K.H., Penitenti, M., Ikoma, M.R., Lara, V.S. 2015. Aging does not affect the ability of human monocyte-derived dendritic cells to phagocytose Candida albicans. Aging Clin Exp Res 27, 785.
  • Plaine, A., Yáñez, A., Murciano, C., Gaillardin, C., Gil, M.L., Richard, M.L., Gozalbo, D. 2008. Enhanced proinflammatory response to the Candida albicans gpi7 null mutant by murine cells. Microbes Infect 10, 382.
  • Rossato, L., Santos, S.S.D., Ferreira, L.G., de Almeida, S.R. 2019. The importance of Toll-like receptor 4 during experimental Sporothrix brasiliensis infection. Med Mycol 57, 489.
  • Rossato, L., Silvana Dos Santos, S., Ferreira, L.G., Rogério de Almeida, S. 2019. The impact of the absence of Toll-like receptor-2 during Sporothrix brasiliensis infection. J Med Microbiol 68, 87.
There is no Supplemental content for this article.

How to Cite This

Yesilyurt Sölen, E. . (2022). The effects of Candida albicans and Candida krusei on expression of toll-like receptors and chemokine receptors by dendritic cells. Jurnal Teknologi Laboratorium, 11(2). https://doi.org/10.29238/teknolabjournal.v11i2.353

Article Metrics

Download Statistics


Download data is not yet available.


Metrics Loading ...

Other Statistics

Verify authenticity via CrossMark

Copyright and Permissions

Creative Commons License

This work is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License.

Publishing your paper with Jurnal Teknologi Laboratorium (JTL) means that the author or authors retain the copyright in the paper. JTL granted an exclusive reuse license by the author(s), but the author(s) are able to put the paper onto a website, distribute it to colleagues, give it to students, use it in your thesis etc, even commercially. The author(s) can reuse the figures and tables and other information contained in their paper published by JTL in future papers or work without having to ask anyone for permission, provided that the figures, tables or other information that is included in the new paper or work properly references the published paper as the source of the figures, tables or other information, and the new paper or work is not direct at private monetary gain or commercial advantage.

JTL journal provides immediate open access to its content on the principle that making research freely available to the public supports a greater global exchange of knowledge. This journal is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License. This license lets others remix, transform, and build upon the material for any purpose, even commercially.

JTL journal Open Access articles are distributed under this Creative Commons Attribution-ShareAlike 4.0 International License (CC BY-SA). Articles can be read and shared for All purposes under the following conditions:

  • BY: You must give appropriate credit, provide a link to the license, and indicate if changes were made. You may do so in any reasonable manner, but not in any way that suggests the licensor endorses you or your use.
  • SA:  If you remix, transform, or build upon the material, you must distribute your contributions under the same license as the original.

Data Availability