Increment of interleukin 6, tumour necrosis factor alpha, nitric oxide, C-reactive protein and apoptosis in dengue

被引:57
作者
Levy, Alegria [1 ]
Valero, Nereida [1 ]
Marina Espina, Luz [1 ]
Anez, German [1 ]
Arias, Julia [1 ]
Mosquera, Jesus [1 ]
机构
[1] Univ Zulia, Fac Med, Inst Invest Clin Dr Americo Negrette, Maracaibo 4011, Venezuela
关键词
Dengue; Cytokines; Complement; Apoptosis; Monocytes; Venezuela; HEMORRHAGIC-FEVER; VIRUS-INFECTION; IN-VITRO; CYTOKINES; PATHOGENESIS; ACTIVATION; SEVERITY; CHILDREN; SEPSIS; TYPE-2;
D O I
10.1016/j.trstmh.2009.06.013
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
This study evaluated the levels of TNF alpha, IL-6, IL-1 beta, nitric oxide (NO), CRP, C3 and apoptosis in 36 patients with dengue fever (DF), 34 patients with dengue haemorrhagic fever (DHF) and in virus-infected monocyte cultures. IL-6, TNF alpha, NO (nitrites) and CRP levels were increased and C3 diminished in patients with DF and DHF. IL-6, TNF alpha, CPR and C3 values were associated with disease severity (DHF). Nitrite content was incremented in DF patients. TNF alpha, NO and CRP levels were associated with secondary infection. IL-6 and CRP levels were associated with dengue virus type 4 (DENV-4) and DENV-2, respectively. Low levels of C3 were associated with DENV-2 and DENV-4 infections. Similarly, increased content of TNFa, IL-6 and nitrites were observed in supernatants from infected monocyte cultures. IL-6 was associated with DENV-4 infection. The different virus serotypes induced apoptosis in monocyte cultures. Dengue infection did not induce elevated IL-1 beta production, either in patients or in infected cultures. These results suggest that TNF alpha, IL-6, NO and CRP are involved in dengue infection and that monocytes could be an important source of cytokine and NO production. (c) 2009 Royal Society of Tropical Medicine and Hygiene. Published by Elsevier Ltd. All rights reserved.
引用
收藏
页码:16 / 23
页数:8
相关论文
共 30 条
[1]   The role of inflammation in vascular insulin resistance with focus on IL-6 [J].
Andersen, K. ;
Pedersen, B. K. .
HORMONE AND METABOLIC RESEARCH, 2008, 40 (09) :635-639
[2]   Differential proinflammatory and angiogenesis-specific cytokine production in human pulmonary endothelial cells, HPMEC-ST1.6R infected with dengue-2 and dengue-3 virus [J].
Azizan, Azliyati ;
Sweat, James ;
Espino, Carlos ;
Gemmer, Jennifer ;
Stark, Lillian ;
Kazanis, Deno .
JOURNAL OF VIROLOGICAL METHODS, 2006, 138 (1-2) :211-217
[3]   Multiplex cytokine profile from dengue patients: MIP-1beta and IFN-gamma as predictive factors for severity [J].
Bozza, Fernando A. ;
Cruz, Oswaldo G. ;
Zagne, Sonia Mo ;
Azeredo, Elzinandes L. ;
Nogueira, Rita M. R. ;
Assis, Edson F. ;
Bozza, Patricia T. ;
Kubelka, Claire F. .
BMC INFECTIOUS DISEASES, 2008, 8 (1)
[4]   Nitric oxide radical suppresses replication of wild-type dengue 2 viruses in vitro [J].
Charnsilpa, W ;
Takhampunya, R ;
Endy, TP ;
Mammen, MP ;
Libraty, DH ;
Ubol, S .
JOURNAL OF MEDICAL VIROLOGY, 2005, 77 (01) :89-95
[5]  
Chaturvedi UC, 2000, FEMS IMMUNOL MED MIC, V28, P183, DOI 10.1111/j.1574-695X.2000.tb01474.x
[6]   CROSSED IMMUNOELECTROPHORESIS FOR THE DETECTION OF SPLIT PRODUCTS OF THE 3RD COMPLEMENT COMPONENT IN DENGUE HEMORRHAGIC-FEVER .2. INVITRO ACTIVATION BY DENGUE VIRAL-ANTIGEN [J].
CHURDBOONCHART, V ;
BHAMARAPRAVATI, N ;
YOKSAN, S .
AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE, 1984, 33 (06) :1239-1247
[7]   Increased apoptosis and expression of tumor necrosis factor-αcaused by infection of cultured human monocytes with dengue virus [J].
Espina, LM ;
Valero, NJ ;
Hernández, JM ;
Mosquera, JA .
AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE, 2003, 68 (01) :48-53
[8]   TNF-α-308A allele, a possible severity risk factor of hemorrhagic manifestation in dengue fever patients [J].
Fernández-Mestre, MT ;
Gendzekhadze, K ;
Rivas-Vetencourt, P ;
Layrisse, Z .
TISSUE ANTIGENS, 2004, 64 (04) :469-472
[9]   RETRACTED: NO-mesalamine protects colonic epithelial cells against apoptotic damage induced by proinflammatory cytokines (Retracted Article. See vol 297, pg G860, 2009) [J].
Fiorucci, S ;
Distrutti, E ;
Ajuebor, MN ;
Mencarelli, A ;
Mannucci, R ;
Palazzetti, B ;
Del Soldato, P ;
Morelli, A ;
Wallace, JL .
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY, 2001, 281 (03) :G654-G665
[10]  
Hack CE, 1997, ADV IMMUNOL, V66, P101, DOI 10.1016/S0065-2776(08)60597-0