Abstract
A cytokine storm is an abnormal discharge of soluble mediators following an inappropriate inflammatory response that leads to immunopathological events. Cytokine storms can occur after severe infections as well as in non-infectious situations where inflammatory cytokine responses are initiated, then exaggerated, but fail to return to homeostasis. Neutrophils, macrophages, mast cells, and natural killer cells are among the innate leukocytes that contribute to the pathogenesis of cytokine storms. Neutrophils participate as mediators of inflammation and have roles in promoting homeostatic conditions following pathological inflammation. This review highlights the advances in understanding the mechanisms governing neutrophilic inflammation against viral and bacterial pathogens, in cancers, and in autoimmune diseases, and how neutrophils could influence the development of cytokine storm syndromes. Evidence for the destructive potential of neutrophils in their capacity to contribute to the onset of cytokine storm syndromes is presented across a multitude of clinical scenarios. Further, a variety of potential therapeutic strategies that target neutrophils are discussed in the context of suppressing multiple inflammatory conditions.
Highlights
The concept of a cytokine storm was first identified in acute graft-versus-host disease following the transplant of hematopoietic stem cells [1]
Neutrophils employ a multifaceted range of tactics to combat an diverse range of pathogens and detrimental clinical manifestations to promote restoration, including but not limited to phagocytosis, the formation of extracellular traps, the production of cytokines such as IFNs, and the modulation of innate lymphoid cells and lymphocytes to drive long-term adaptive responses against a broad spectrum of ailments
In this review we have highlighted the destructive potential of neutrophils (Figure 1) in their capacity to contribute to the induction of auto-immune disorders, augment the progression of cancers, cause massive tissue injuries in viral infections and, promote the onset of Cytokine storm syndrome (CSS) across a multitude of clinical scenarios
Summary
The concept of a cytokine storm was first identified in acute graft-versus-host disease following the transplant of hematopoietic stem cells [1]. Cytokine storm syndrome (CSS) is used as a general term entailing diverse immune-related dysregulations that are triggered by distinct driving factors and result in systemic inflammation, clinical symptoms, and sometimes multiple organ dysfunction [2]. The production of cytokines is commonly controlled by anti-inflammatory mechanisms As a result, these molecules do not usually modulate inflammation much beyond the site of infection and/or damage [2]. The innate leukocytes, namely neutrophils, monocytes, macrophages, dendritic cells, and natural killer (NK) cells are among the first line of defense against pathogens and tissue damage and are known to be involved in cytokine secretion and inflammatory reactions [14]. An overview of the potential pharmacologic interventions against CSS that target neutrophils through distinct mechanisms will be discussed
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