OBJECTIVESepsis is defined as life-threatening organ dysfunction due to a dysregulated host response to infection. In this article, we reviewed the correlation between neutrophil dysfunction and sepsis.

DATA SOURCESArticles published up to May 31, 2016, were selected from the PubMed databases, with the keywords of "neutrophil function", "neutrophil dysfunction", and "sepsis".

STUDY SELECTIONArticles were obtained and reviewed to analyze the neutrophil function in infection and neutrophil dysfunction in sepsis.

RESULTSWe emphasized the diagnosis of sepsis and its limitations. Pathophysiological mechanisms involve a generalized circulatory, immune, coagulopathic, and/or neuroendocrine response to infection. Many studies focused on neutrophil burst or cytokines. Complement activation, impairment of neutrophil migration, and endothelial lesions are involved in this progress. Alterations of cytokines, chemokines, and other mediators contribute to neutrophil dysfunction in sepsis.

CONCLUSIONSSepsis represents a severe derangement of the immune response to infection, resulting in neutrophil dysfunction. Neutrophil dysfunction promotes sepsis and even leads to organ failure. Mechanism studies, clinical practice, and strategies to interrupt dysregulated neutrophil function in sepsis are desperately needed.

Animals ; Cell Movement ; physiology ; Humans ; Neutrophils ; physiology ; Sepsis ; physiopathology

Asthma ; pathology ; Basophils ; physiology ; Bronchi ; pathology ; Humans ; Neutrophils ; physiology

BACKGROUNDPolymorphonuclear neutrophil (PMN), one of the most important inflammatory cells, functions throughout the initiation, progression and resolution of inflammation. This study aimed at investigating the relationship between PMN apoptosis and the lung injury after chest impact trauma.

METHODSPMNs were purified from rabbits subjected to the chest impact trauma and their apoptosis, necrosis, survival and respiratory burst were detected by flow cytometry. Meanwhile, lactate dehydrogenase and (LDH) [Ca2+]i were measured.

RESULTSThe delayed apoptosis of PMNs in bronchoalveolar lavage fluid was observed from 2 hours to 12 hours after trauma, and viable cells increased. Respiratory burst of PMNs in bronchoalveolar lavage fluid was increased significantly from 2 hours with the peak at 8 hours. Meanwhile, lactate dehydrogenase in bronchoalveolar lavage fluid was higher than that in control (P < 0.05) from 4 hours to 24 hours, and intracellular free Ca2+ in PMN was increased temporarily.

CONCLUSIONSRetention of PMN in tissues and the abnormality in apoptotic pathway inevitably generate persistent activation of PMN and excessive release of toxic substances, resulting in tissue injury. The temporary increase of intracellular free Ca2+ may be responsible for the delayed apoptosis of PMN.

Animals ; Apoptosis ; physiology ; Lung Injury ; Neutrophils ; physiology ; Rabbits ; Respiratory Burst ; physiology ; Thoracic Injuries ; complications

OBJECTIVETo investigate the effects of fresh and preserved amniotic membrane on polymorphonuclear neutrophils (PMNs) so as to understand the anti-inflammatory mechanism of amniotic membrane transplantation.

METHODSConditioned medium was collected 48 hours after fresh or preserved amnions were cultured in DMEM and 5% CO(2) at 37 degrees C. Then, polymorphonuclear cells were cultured in conditioned culture or DMEM. Fluorescent microscopy with 4',6-diamidino-2-phenylindole (DAPI) staining and cytometry were performed 6, 9, 12, and 15 hours later.

RESULTSApoptotic neutrophils were found in each group at different time points. The percentage of apoptotic cells at 6, 9, 12, and 15 hours after culture in the fresh and preserved amnion groups and the control group was 17.3%, 24.4%, 29.8%, 37.1%, and 16.2%, 20.1%, 23.7%, 27.7%, and 10.2%, 13.7%, 21.1%, 26.4%, respectively (t test, P(1) < 0.01, P(2) < 0.01 and P(3) < 0.01).

CONCLUSIONAmniotic membrane can accelerate apoptosis of polymorphonuclear neutrophils, reduce inflammation, and prevent ocular surface collagen from resolution, indicating that fresh amnion might have a stronger effect than preserved amnion.

Amnion ; physiology ; Apoptosis ; Cells, Cultured ; Neutrophils ; cytology ; immunology

Neutrophil extracellular traps (NETs) represent a form of cell death distinct from apoptosis or necrosis. The imbalance between the formation and degradation of NETs has long been considered to be closely associated with the activity of autoimmune diseases such as systemic lupus erythematous (SLE). Reactive oxygen species derived from the nicotinamide adenine dinucleotide phosphate oxidase pathway or mitochondrial DNA pathway play a key role in the primary stage of NETs formation. The exposure or delayed degradation of abundant autoantigens, such as double-strand DNA, caused by abnormal activation of neutrophils can induce autoantibody to form immune complexes that deposit in local tissues and then induce the plasmacytoid dendritic cells to secrete the interferon alpha and other inflammatory factors. Those inflammatory factors will eventually cause endothelial cell injury. In order to provide a theoretical basis for targeted therapy and diagnosis of childhood-onset SLE, this paper reviews the role of NETs in the pathogenesis of SLE.
Extracellular Traps ; Humans ; Lupus Erythematosus, Systemic ; etiology ; therapy ; Neutrophils ; physiology

Sepsis remains one of the leading causes of death globally, in spite of advanced developments in intensive care and better understandings of pathophysiology related to sepsis. There is no special treatment or drug available for sepsis, currently. Under normal circumstances, neutrophil is a major player in acute infection control. However, during sepsis, the migration abilities and antimicrobial functions of neutrophils are impaired, resulting in a dysregulated immune response. Recent studies have indeed demonstrated that blocking or reversing neutrophil migration and impaired antibacterial function can improve the outcomes in septic animal models. This article systemically synthesized information regarding related factors and signaling involved in the functions of neutrophils in sepsis. This review also discussed the possibility that neutrophils be used as a marker for specific diagnosis and/or prediction of the outcomes of sepsis.
Animals ; Neutrophils/physiology* ; Chemotaxis ; Chemotaxis, Leukocyte ; Sepsis ; Cell Movement

Neutrophils are important effector cells against protozoan extracellular parasite Entamoeba histolytica, which causes amoebic colitis and liver abscess in human beings. Apoptotic cell death of neutrophils is an important event in the resolution of inflammation and parasite's survival in vivo. This study was undertaken to investigate the ultrastructural aspects of apoptotic cells during neutrophil death triggered by Entamoeba histolytica. Isolated human neutrophils from the peripheral blood were incubated with or without live trophozoites of E. histolytica and examined by transmission electron microscopy (TEM). Neutrophils incubated with E. histolytica were observed to show apoptotic characteristics, such as compaction of the nuclear chromatin and swelling of the nuclear envelop. In contrast, neutrophils incubated in the absence of the amoeba had many protrusions of irregular cell surfaces and heterogenous nuclear chromatin. Therefore, it is suggested that Entamoeba-induced neutrophil apoptosis contribute to prevent unwanted tissue inflammation and damage in the amoeba-invaded lesions in vivo.
Animals ; Apoptosis/*physiology ; Entamoeba histolytica/*physiology ; Host-Parasite Relations/physiology ; Humans ; In Vitro ; Neutrophils/physiology/*ultrastructure ; Research Support, Non-U.S. Gov't

Neutrophils play a critical role in ventilation-induced lung injury. This study was aimed to investigate the characteristics of neutrophils influx in lungs induced by high tidal volume ventilation. Anaesthetized rats were randomly divided into low tidal volume ventilation group (Vt: 7 mL/kg, LV group) or high tidal volume ventilation group (Vt: 42 mL/kg, HV group) (n=40 in each). Rats in each group were ventilated for 0, 60, 90, 120 and 240 min. The wet/dry lung weight ratio (W/D) was measured. The levels of macrophage inflammatory protein-2 (MIP-2) and tumor necrosis factor-α (TNF-α), and the activity of myeloperoxidase (MPO) were detected by enzyme-linked immunosorbent assay (ELISA). The number of neutrophils in bronchoalveolar lavage fluid (BALF) was counted after Wright's staining, and the percentage of netrophils in lung tissues calculated. Histopatholgical examination was used to observe the changes of lung tissues after different ventilations. The results showed that the W/D weight ratio was increased, and the levels of MIP-2 and TNF-α significantly enhanced in HV group at 90, 120 and 240 min. Neutrophils in BALF and the neutrophil percentage in lung tissues were also elevated at 120 and 240 min, which coincided with the enhanced activity of MPO in HV group. The lung injury was significantly related with the ventilation time and the infiltration of neutrophils in lungs in HV group. In conclusion, in ventilation-induced lung injury, neutrophil infiltration is present in a time-dependent manner and associated with the aggravated lung injury. Pulmonary structural damage may be the main reason for ventilation-induced lung injury.
Animals ; Lung ; physiopathology ; Lung Injury ; physiopathology ; Male ; Neutrophil Infiltration ; physiology ; Neutrophils ; physiology ; Rats ; Rats, Sprague-Dawley

Asthma ; physiopathology ; Humans ; Inflammation ; etiology ; Matrix Metalloproteinase 9 ; analysis ; physiology ; Neutrophil Activation ; Neutrophils ; physiology ; Transforming Growth Factor beta ; physiology

Human polymorphonuclear leukocytes (PMN) migrate into tissues in response to chemoattractants, yet it is not known whether this process alters the functional capabilities of the PMN. Using recombinant human interleukin-8 (rHIL-8, 100 ng/ml) as a stimulus, we compared a population of PMN that migrated through a polyvinylpyrrolidone-coated polycarbonate filter containing 8.0 microns diameter pores with PMN stimulated in suspension. PMN were analyzed by flow cytometry according to functional and phenotypic criteria. CD11b/CD16 expression was unaltered by chemotaxis. In contrast, chemotaxis enhanced phagocytosis of E. coli, independent of opsonization with IgG. Similarly, chemotaxis increased baseline hydrogen peroxide production. We conclude that the chemotactic motion of PMN "primes" the cell for increased oxidative burst activity and augments the ability of PMN to ingest bacteria. This increased functional capability is distinct from rHIL-8 stimulation and appears to be independent of complement-and Fc-receptor expression.
Antigens, CD/analysis ; Chemotaxis, Leukocyte/*physiology ; Escherichia coli/immunology ; Humans ; Neutrophils/physiology ; Phagocytosis/physiology ; Phenotype ; Receptors, IgG/analysis ; Respiratory Burst/physiology