This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Blasi, E Articles by Bistoni, F Search for Related Content PubMed PubMed Citation Articles by Blasi, E Articles by Bistoni, F

 Previous Article  |  Next Article 

Infection and Immunity, April 1994, p. 1199-1206, Vol. 62, No. 4
0019-9567/1994/$04.00+0     DOI:

research-article

Tumor necrosis factor as an autocrine and paracrine signal controlling the macrophage secretory response to Candida albicans.

Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Italy.

ABSTRACT

We have previously demonstrated that the hyphal form of Candida albicans (H-Candida), but not the yeast form (Y-Candida), acts as a macrophage-stimulating agent. The early response (1 to 3 h) of the macrophage cell line ANA-1 to H-Candida results in enhanced tumor necrosis factor (TNF) transcription and production. Here we show that when coincubation times are prolonged (3 to 24 h), Y-Candida also exhibits stimulatory properties. This phenomenon has been ascribed to the occurrence of the dimorphic transition, as demonstrated by microscopic evaluation of the cultures and by experiments in which both killed Y-Candida and the agerminative strain C. albicans PCA-2 failed to induce cytokine production. TNF produced in response to H-Candida acts as an autocrine and paracrine signal controlling the macrophage secretory response to C. albicans. In fact, addition of anti-TNF polyclonal antibodies to the coculture of ANA-1 macrophages and H-Candida results in a marked and time-dependent decrease of TNF transcript levels. Moreover, pretreatment of macrophages with recombinant TNF for 3 h enhances TNF and induces interleukin-1 production in response to both forms of Candida, while pretreatment for 18 h renders macrophages refractory to any stimuli. Interestingly, the kinetics of interleukin-1 transcription and secretion in response to H-Candida are delayed with respect to those of TNF. Overall, these data indicate that TNF, produced by macrophages in response to H-Candida, regulates its own production as well as that of other soluble factors, thus suggesting that this cytokine plays multiple roles in the immune mechanisms involved in Candida infection.

This article has been cited by other articles:

• Navarathna, D. H. M. L. P., Nickerson, K. W., Duhamel, G. E., Jerrels, T. R., Petro, T. M. (2007). Exogenous Farnesol Interferes with the Normal Progression of Cytokine Expression during Candidiasis in a Mouse Model. Infect. Immun. 75: 4006-4011 [Abstract] [Full Text]  
• Renna, M. S., Correa, S. G., Porporatto, C., Figueredo, C. M., Aoki, M. P., Paraje, M. G., Sotomayor, C. E. (2006). Hepatocellular apoptosis during Candida albicans colonization: involvement of TNF-{alpha} and infiltrating Fas-L positive lymphocytes. Int Immunol 18: 1719-1728 [Abstract] [Full Text]  
• Correa, S. G., Rodriguez-Galan, M. C., Salido-Renteria, B., Cano, R., Cejas, H., Sotomayor, C. E. (2004). High dissemination and hepatotoxicity in rats infected with Candida albicans after stress exposure: potential sensitization to liver damage. Int Immunol 16: 1761-1768 [Abstract] [Full Text]  
• Rodriguez-Galan, M. C., Sotomayor, C., Costamagna, M. E., Cabanillas, A. M., Renteria, B. S., Masini-Repiso, A. M., Correa, S. (2003). Immunocompetence of macrophages in rats exposed to Candida albicans infection and stress. Am. J. Physiol. Cell Physiol. 284: C111-C118 [Abstract] [Full Text]  
• Steele, C., Fidel, P. L. Jr. (2002). Cytokine and Chemokine Production by Human Oral and Vaginal Epithelial Cells in Response to Candida albicans. Infect. Immun. 70: 577-583 [Abstract] [Full Text]