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Anti-Neutrophil Elastase Rabbit pAb antibody

RRID:AB_212213

Antibody ID

AB_212213

Target Antigen

Human Neutrophil Elastase human

Proper Citation

(Millipore Cat# 481001-1ML, RRID:AB_212213)

Clonality

polyclonal antibody

Comments

seller recommendations: ELISA, Immunoblotting, Immunoelectrophoresis, Immunoprecipitation

Host Organism

rabbit

Vendor

Millipore

Cat Num

481001-1ML

Publications that use this research resource

Diverse stimuli engage different neutrophil extracellular trap pathways.

  • Kenny EF
  • Elife
  • 2017 Jun 2

Literature context:


Abstract:

Neutrophils release neutrophil extracellular traps (NETs) which ensnare pathogens and have pathogenic functions in diverse diseases. We examined the NETosis pathways induced by five stimuli; PMA, the calcium ionophore A23187, nigericin, Candida albicans and Group B Streptococcus. We studied NET production in neutrophils from healthy donors with inhibitors of molecules crucial to PMA-induced NETs including protein kinase C, calcium, reactive oxygen species, the enzymes myeloperoxidase (MPO) and neutrophil elastase. Additionally, neutrophils from chronic granulomatous disease patients, carrying mutations in the NADPH oxidase complex or a MPO-deficient patient were examined. We show that PMA, C. albicans and GBS use a related pathway for NET induction, whereas ionophores require an alternative pathway but that NETs produced by all stimuli are proteolytically active, kill bacteria and composed mainly of chromosomal DNA. Thus, we demonstrate that NETosis occurs through several signalling mechanisms, suggesting that extrusion of NETs is important in host defence.

Funding information:
  • NIGMS NIH HHS - R35 GM118112()

Lactoferrin Suppresses Neutrophil Extracellular Traps Release in Inflammation.

  • Okubo K
  • EBioMedicine
  • 2016 Aug 2

Literature context:


Abstract:

Neutrophils are central players in the innate immune system. They generate neutrophil extracellular traps (NETs), which protect against invading pathogens but are also associated with the development of autoimmune and/or inflammatory diseases and thrombosis. Here, we report that lactoferrin, one of the components of NETs, translocated from the cytoplasm to the plasma membrane and markedly suppressed NETs release. Furthermore, exogenous lactoferrin shrunk the chromatin fibers found in released NETs, without affecting the generation of oxygen radicals, but this failed after chemical removal of the positive charge of lactoferrin, suggesting that charge-charge interactions between lactoferrin and NETs were required for this function. In a model of immune complex-induced NET formation in vivo, intravenous lactoferrin injection markedly reduced the extent of NET formation. These observations suggest that lactoferrin serves as an intrinsic inhibitor of NETs release into the circulation. Thus, lactoferrin may represent a therapeutic lead for controlling NETs release in autoimmune and/or inflammatory diseases.