Neutrophil paralysis in sepsis.
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.
Alves-Filho
José C
JC
Department of Pharmacology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, São Paulo, Brazil. jcafilho@usp.br
Spiller
Fernando
F
Cunha
Fernando Q
FQ
D000818:Animals; D002634:Chemotaxis, Leukocyte / Q000502:physiology; D016207:Cytokines / Q000502:physiology; D006801:Humans; D007239:Infections / Q000276:immunology / Q000503:physiopathology; D018836:Inflammation Mediators / Q000502:physiology; D009102:Multiple Organ Failure / Q000209:etiology / Q000503:physiopathology; D009504:Neutrophils / Q000502:physiology*; D052247:Nitric Oxide Synthase Type II / Q000502:physiology; D009928:Organ Specificity; D047495:PPAR gamma / Q000502:physiology; D018805:Sepsis / Q000150:complications / Q000276:immunology / Q000503:physiopathology* / Q000628:therapy; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology / Q000503:physiopathology; D051193:Toll-Like Receptors / Q000502:physiology
D016207:Cytokines; D018836:Inflammation Mediators; D047495:PPAR gamma; D051193:Toll-Like Receptors; D052247:Nitric Oxide Synthase Type II