Into the Eye of the Cytokine Storm

Abstract

SUMMARY The cytokine storm has captured the attention of the public and the scientific community alike, and while the general notion of an excessive or uncontrolled release of proinflammatory cytokines is well known, the concept of a cytokine storm and the biological consequences of cytokine overproduction are not clearly defined. Cytokine storms are associated with a wide variety of infectious and noninfectious diseases. The term was popularized largely in the context of avian H5N1 influenza virus infection, bringing the term into popular media. In this review, we focus on the cytokine storm in the context of virus infection, and we highlight how high-throughput genomic methods are revealing the importance of the kinetics of cytokine gene expression and the remarkable degree of redundancy and overlap in cytokine signaling. We also address evidence for and against the role of the cytokine storm in the pathology of clinical and infectious disease and discuss why it has been so difficult to use knowledge of the cytokine storm and immunomodulatory therapies to improve the clinical outcomes for patients with severe acute infections.

The comparison of Th1, Th2, Th9, Th17 and Th22 cytokine profiles in acute and chronic HIV-1 infection

“…In time, constant viral replication and immune activation cause further decrease in CD4+ T-cell counts, immune system loses control over infection leading to opportunistic infections, malignancies and death of untreated individuals [3]. Cytokines are biological response modifiers synthesized by cells of innate and adaptive immunity that are important in intercellular communication and regulation of immune reactions [9], [10], [11] and [12]. Effector functions of CD4+ T-cells depend on cytokine immunity.…”

A case of thyroid storm with a markedly elevated level of circulating soluble interleukin-2 receptor complicated by multiple organ failure and disseminated intravascular coagulation syndrome

“…MOF has been shown to develop from a heterogeneous disease population such as severe infection, shock, trauma, burns, and pancreatitis due to inappropriate generalized inflammatory responses in the host to various acute insults [12,13]. Illnesses that lead to the development of MOF are well-known triggers for TS [1,2].…”

Tumor Necrosis Factor-Alpha as Biomarkers of Exposure to Indoor Pollutants Among Primary School Children in Klang Valley

“…TNF-α is pro-inflammatory mediators, which may act as intermediate to alert the body of higher susceptibility (Lo Tam Loi et al, 2013;Tisoncik et al, 2012) especially in the lung (Sullivan et al, 2009). Furthermore, exposures to particulate air pollution may lead to adverse health effects which may induce airway cell damage (Revai et al, 2009).…”