Early expression of local cytokines during systemic Candida albicans infection in a murine intravenous challenge model

被引:15
作者
Chin, Voon Kin [1 ]
Foong, Kuan Jeang [1 ]
Maha, Abdullah [2 ]
Rusliza, Basir [3 ]
Norhafizah, Mohtarrudin [2 ]
Chong, Pei Pei [1 ,4 ]
机构
[1] Univ Putra Malaysia, Fac Med & Hlth Sci, Dept Biomed Sci, Serdang 43400, Selangor, Malaysia
[2] Univ Putra Malaysia, Fac Med & Hlth Sci, Dept Pathol, Serdang 43400, Selangor, Malaysia
[3] Univ Putra Malaysia, Fac Med & Hlth Sci, Dept Human Anat, Serdang 43400, Selangor, Malaysia
[4] Natl Univ Singapore, Dept Microbiol, Ctr Translat Med, Translat Infect Dis Program, Singapore 117597, Singapore
关键词
Candida albicans; cytometric bead array analysis; ELISA; cytokines;
D O I
10.3892/br.2014.365
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Local cytokine production is a significant indicator for disease pathogenesis or progression. Previous studies on cytokine production during systemic Candida albicans (C. albicans) infection were solely on kidney or single cell type interaction with C. albicans. Therefore, the present study aimed to assess the early cytokine expression of various target organs (kidney, spleen and brain) over a 72-h time course during systemic C. albicans infection. The local cytokine profiles of the target organs during systemic C. albicans infection were measured by cytometric bead array and ELISA analysis. The results demonstrated that interleukin-6 (IL-6) and IL-2 were statistically significant (P<0.05) in the spleen at 24 and 72 h post-infection, whereas in the kidney, IL-6 and tumor necrosis factor-a (TNF-a) were statistically significant (P<0.05) at 24 and 72 h post-infection and CXCL-1 and transforming growth factor-beta (TGF-beta) were statistically significant (P<0.05) at 72 h post-infection. In the brain, IL-6 and TNF-a were statistically significant (P<0.05) at 24 and 72 h post-infection, whereas TGF-(beta) was statistically significant (P<0.05) at 72 h post-infection. These findings demonstrate that host immune responses were varied among target organs during systemic C. albicans infection. This could be important for designing targeted immunotherapy against this pathogen through immunomodulatory approaches in future exploratory research.
引用
收藏
页码:869 / 874
页数:6
相关论文
共 39 条
[1]  
Abbas AK, 1997, CELLULAR MOL IMMUNOL, P15
[2]   PRODUCTION AND FUNCTION OF CYTOKINES IN NATURAL AND ACQUIRED-IMMUNITY TO CANDIDA-ALBICANS INFECTION [J].
ASHMAN, RB ;
PAPADIMITRIOU, JM .
MICROBIOLOGICAL REVIEWS, 1995, 59 (04) :646-&
[3]   TRANSFORMING GROWTH-FACTOR-BETA AS A VIRULENCE MECHANISM FOR LEISHMANIA-BRAZILIENSIS [J].
BARRAL, A ;
BARRALNETTO, M ;
YONG, EC ;
BROWNELL, CE ;
TWARDZIK, DR ;
REED, SG .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1993, 90 (08) :3442-3446
[4]   GROWTH-INHIBITION OF CANDIDA-ALBICANS BY INTERLEUKIN-2-ACTIVATED SPLENOCYTES [J].
BENO, DWA ;
MATHEWS, HL .
INFECTION AND IMMUNITY, 1992, 60 (03) :853-863
[5]   Mechanisms of disease:: Role of transforming growth factor β in human disease. [J].
Blobe, GC ;
Schiemann, WP ;
Lodish, HF .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 342 (18) :1350-1358
[6]   Comparison of pathogenesis and host immune responses to Candida glabrata and Candida albicans in systemically infected immunocompetent mice [J].
Brieland, J ;
Essig, D ;
Jackson, C ;
Frank, D ;
Loebenberg, D ;
Menzel, F ;
Arnold, B ;
DiDomenico, B ;
Hare, R .
INFECTION AND IMMUNITY, 2001, 69 (08) :5046-5055
[7]   Neutrophil chemokines KC and macrophage-inflammatory protein-2 are newly synthesized by tissue macrophages using distinct TLR signaling pathways [J].
De Filippo, Katia ;
Henderson, Robert B. ;
Laschinger, Melanie ;
Hogg, Nancy .
JOURNAL OF IMMUNOLOGY, 2008, 180 (06) :4308-4315
[8]  
DEKOSSODO S, 1993, J IMMUNOL, V151, P4811
[9]   Microcoding and flow cytometry as a high-throughput fungal identification system for Malassezia species [J].
Diaz, Mara R. ;
Boekhout, Teun ;
Theelen, Bart ;
Bovers, Marjan ;
Cabanes, Francisco J. ;
Fell, Jack W. .
JOURNAL OF MEDICAL MICROBIOLOGY, 2006, 55 (09) :1197-1209
[10]   Proinflammatory cytokines [J].
Dinarello, CA .
CHEST, 2000, 118 (02) :503-508