Determination of tumor necrosis factor-alpha levels in dengue virus infected patients by sensitive biotin-streptavidin enzyme-linked immunosorbent assay

Kittigul, Leera; Temprom, W; Sujirarat, Dusit; Kittigul, Chaivat

doi:10.1016/s0166-0934(00)00215-9

Cited by 50 publications

(39 citation statements)

References 16 publications

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“…High levels of TNF-α were also observed in sera of all patients with dengue infection, with the highest values found in patients with DSS (93). Furthermore, the elevation of TNF-α in the serum has been reported to be strongly associated with clinical disease progression from DF to DSS (94,95). Furthermore, anti-TNF-α antibody has been reported to be an effective treatment to reduce mortality associated with DV infection (96).…”

Section: Figurementioning

confidence: 99%

Activation of MDL-1 (CLEC5A) on immature myeloid cells triggers lethal shock in mice

Cheung¹,

Shen²,

Phillips³

et al. 2011

J. Clin. Invest.

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Systemic inflammatory response syndrome (SIRS) is a potentially lethal condition, as it can progress to shock, multi-organ failure, and death. It can be triggered by infection, tissue damage, or hemorrhage. The role of tissue injury in the progression from SIRS to shock is incompletely understood. Here, we show that treatment of mice with concanavalin A (ConA) to induce liver injury triggered a G-CSF-dependent hepatic infiltration of CD11b + Gr-1 + Ly6G + Ly6C + immature myeloid cells that expressed the orphan receptor myeloid DAP12-associated lectin-1 (MDL-1; also known as CLEC5A). Activation of MDL-1 using dengue virus or an agonist MDL-1-specific antibody in the ConA-treated mice resulted in shock. The MDL-1 + cells were pathogenic, and in vivo depletion of MDL-1 + cells provided protection. Triggering MDL-1 on these cells induced production of NO and TNF-α, which were found to be elevated in the serum of treated mice and required for MDL-1-induced shock. Surprisingly, MDL-1-induced NO and TNF-α production required eNOS but not iNOS. Activation of DAP12, DAP10, Syk, PI3K, and Akt was critical for MDL-1-induced shock. In addition, Akt physically interacted with and activated eNOS. Therefore, triggering of MDL-1 on immature myeloid cells and production of NO and TNF-α may play a critical role in the pathogenesis of shock. Targeting the MDL-1/Syk/PI3K/Akt/eNOS pathway represents a potential new therapeutic strategy to prevent the progression of SIRS to shock.

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Section: Figurementioning

confidence: 99%

Activation of MDL-1 (CLEC5A) on immature myeloid cells triggers lethal shock in mice

Cheung¹,

Shen²,

Phillips³

et al. 2011

J. Clin. Invest.

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“…[13][14][15][16] Other studies have suggested that cytokine levels can be used as predictive factors for severity in dengue. 17 High levels of IL-6 have implications for development of pathology in severe dengue, playing an important role in the production of antiplatelet or antiendothelial cell antibodies, as well as elevated levels of tissue plasminogen activator, and a deficiency in coagulation, leading to plasma leakage and bleeding.…”

Section: Introductionmentioning

confidence: 99%

Dengue Patients with Early Hemorrhagic Manifestations Lose Coordinate Expression of the Anti-Inflammatory Cytokine IL-10 with the Inflammatory Cytokines IL-6 and IL-8

Iani¹,

Caldas

Duarte

et al. 2016

The American Society of Tropical Medicine and Hygiene

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Abstract. Dengue is responsible for a wide range of clinical manifestations, ranging from asymptomatic infections to severe cases. The alteration of cytokine levels correlated with clinical characteristics can help determine prognostic markers of the disease and the identification of targets for immunotherapy. We measured the viral load, serotype, and cytokine levels of 212 serum samples from patients with acute dengue infection during days 1-4 after the onset of symptoms. The patients were classified as either with hemorrhagic manifestations (HM) or with no hemorrhagic manifestations (NHM). The cytokines interleukin-6 (IL-6), IL-8, and IL-10 were increased (P < 0.05) in the dengue virus+ group, compared with the control group. A higher viral load (P < 0.05) and IL-6 was detected in the HM group compared with the NHM group. Interestingly, the NHM group demonstrated a significant positive correlation between inflammatory (IL-6 and 8) and anti-inflammatory (IL-10) cytokines, whereas the HM group did not. These findings suggest that a disturbance in the balance of inflammatory cytokines IL-6 and IL-8 with the anti-inflammatory cytokine, IL-10, combined with the high levels of IL-6 and viral load, characterize possible mechanisms related to the formation of HM.

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“…A strong correlation between high concentration of tumor necrosis factor alpha (TNF-␣) in blood and the severity of DHF has been reported. [28][29][30][31] The presence of apoptosis has been suggested to be related to the pathogenesis of DHF, 25,32 and TNF-␣ could be involved in the pathogenesis of DHF by inducing apoptotic processes. 33 NO can protect cells from apoptosis induced by TNF-␣, 34 and in addition, NO has an inhibitory effect on TNF-␣ release from human peripheral blood monocytes.…”

Section: Introductionmentioning

confidence: 99%

Short report: increased level of serum nitric oxide in patients with dengue.

Valero¹,

Espina²,

Áñez³

et al. 2002

The American Journal of Tropical Medicine and Hygiene

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Abstract. Nitric oxide (NO) has been involved in several infectious diseases. Virus dengue is capable of inducing increased levels of NO when cocultured with human Kupffer and spleen cells. However, no reports describe the levels of NO in patients with dengue infection. Increased levels of NO were found in patients with the classic form of the disease; however, in the hemorrhagic form of the disease, similar levels to those of healthy controls were found. In vitro studies showed no increased levels of NO when human platelets were incubated with the virus. Increased NO in classical dengue could be important in the evolution from the nonhemorrhagic to the hemorrhagic forms of dengue.

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Determination of tumor necrosis factor-alpha levels in dengue virus infected patients by sensitive biotin-streptavidin enzyme-linked immunosorbent assay

Cited by 50 publications

References 16 publications

Activation of MDL-1 (CLEC5A) on immature myeloid cells triggers lethal shock in mice

Activation of MDL-1 (CLEC5A) on immature myeloid cells triggers lethal shock in mice

Dengue Patients with Early Hemorrhagic Manifestations Lose Coordinate Expression of the Anti-Inflammatory Cytokine IL-10 with the Inflammatory Cytokines IL-6 and IL-8

Short report: increased level of serum nitric oxide in patients with dengue.

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