Abstract
Sepsis develops when the initial host response is unable to contain the primary infection, resulting in widespread inflammation and multiple organ dysfunction. The impairment of neutrophil migration into the infection site, also termed neutrophil paralysis, is a critical hallmark of sepsis, which is directly related to the severity of the disease. Although the precise mechanism of this phenomenon is not fully understood, there has been much advancement in the understanding of this field. In this review, we highlight the recent insights into the molecular mechanisms of neutrophil paralysis during sepsis.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Chemotaxis, Leukocyte* / physiology
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Cytokines / physiology
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Humans
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Infections / immunology
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Infections / physiopathology
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Inflammation Mediators / physiology
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Multiple Organ Failure / etiology
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Multiple Organ Failure / physiopathology
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Neutrophils / physiology*
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Nitric Oxide Synthase Type II / physiology
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Organ Specificity
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PPAR gamma / physiology
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Sepsis / complications
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Sepsis / immunology
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Sepsis / physiopathology*
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Sepsis / therapy
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Systemic Inflammatory Response Syndrome / etiology
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Systemic Inflammatory Response Syndrome / physiopathology
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Toll-Like Receptors / physiology
Substances
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Cytokines
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Inflammation Mediators
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PPAR gamma
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Toll-Like Receptors
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Nitric Oxide Synthase Type II