Effects of platelet release products on neutrophilic activity in human whole blood

Wu, Bin; Liu, G.; Yube, Kouichi; Ueno, Masaki; Tanaka, Sumiko; Onodera, Masayuki; Jin, Zhongwu; Sakamoto, Haruhiko

doi:10.1007/s00011-009-8230-y

Cited by 13 publications

(8 citation statements)

References 27 publications

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“…In a flow cytometric analysis of phagocytosis using whole blood, plateletrelease products and MAPPs showed the activation of phagocytosis (Wu et al 2009), similar to that observed in experiments using Terasaki microplates.…”

Section: Effects Of Platelet-release Products and Mapps On Neutrophilsupporting

confidence: 75%

“…In some experiments, a flow cytometric study using whole blood was performed to assess phagocytosis (Wu et al 2009). Briefly, 100 μL of heparinized venous blood was mixed with 100 μL of a stimulant prepared in RPMI 1640 supplemented with 1% bovine serum albumin, and the phagocytosis of FITClabeled E. coli (Sigma, St Luis, MO, USA) was assessed by measuring neutrophilassociated fluorescence with a flow cytometer (EPICS ® XL, Coulter Corp., Hialeah, FL, USA).…”

Section: Phagocytosis Assaymentioning

confidence: 99%

“…Deuel et al 1981); phagocytosis by neutrophils and monocytes is enhanced ; enzyme release and O 2 -generation by neutrophils are induced (Laghi et al 1985, Wu et al 2009); lysosomal degranulation is enhanced (Del Mascio et al 1985); the aggregation and cytotoxicity of neutrophils are induced (Boogaerts et al 1986); the adhesion of neutrophils to endothelial cells and nylon fibers is induced (Oryu et al 1996); the expression of some opsonin receptors is up-regulated (Sakamoto et al 1998, Miyabe et al 2004); the apoptosis of neutrophils is inhibited (Andonegui et MAPPs are platelet-derived activators of the phagocytosis of neutrophils that act via Fcγ receptors (Sakamoto & Ooshima 1986). Studies on the characterization of MAPPs and the mechanisms of MAPP activation by the apolipoprotein CIII (Apo CIII)-derived peptide, HATKTAK (Sakamoto et al 2012) will be reviewed herein, and the perspectives of these studies through immunohistochemistry using an antibody against HATKTAK will be described.…”

Section: Introduction/ Backgroundmentioning

confidence: 99%

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The apolipoprotein CIII-derived peptide, HATKTAK, and stimulation of macromolecular activators of phagocytosis from platelets (MAPPs)

Sakamoto

Chiba

Kawauchi

et al. 2017

MRAJ

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We previously reported that activated human platelets release small and large macromolecular activators of phagocytosis from platelets (S-MAPP and L-MAPP, respectively), which enhance Fcγ receptor-mediated phagocytosis by neutrophils. We subsequently investigated the production and release of S-MAPP and L-MAPP by platelets as well as the structure of MAPPs. Experiments using expired platelet concentrates revealed that precursors of MAPPs (dimer or tetramer holo-transferrin) were converted to MAPPs by HATKTAK cleaved from Apo CIII on HDL in or on platelets. Immunohistochemistry showed that a rabbit IgG antibody against HATKTAK visualized not only platelets in blood coagula and thrombi, but also the foamy macrophages and smooth muscle cells of atheroma, some endothelial cells of blood vessels, glomerular filtrate, tubular epithelial cells of kidneys, and some fibers and cell bodies of neurons. HATKTAK appears to be widely distributed in the human body and plays some roles in biological reactions other than lipid metabolism. We herein review the process of investigation and describe perspectives.

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Section: Effects Of Platelet-release Products and Mapps On Neutrophilsupporting

confidence: 75%

Section: Phagocytosis Assaymentioning

confidence: 99%

Section: Introduction/ Backgroundmentioning

confidence: 99%

See 1 more Smart Citation

The apolipoprotein CIII-derived peptide, HATKTAK, and stimulation of macromolecular activators of phagocytosis from platelets (MAPPs)

Sakamoto

Chiba

Kawauchi

et al. 2017

MRAJ

View full text Add to dashboard Cite

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“…Thus, microparticles have been reported to be released in stored platelets [72,73] and have recently been impressively demonstrated in apheresis platelets [74]. In addition, in stored platelets, indirect evidence suggests the release of ATP [75,76,77]. Microparticles have also been detected in fresh frozen/thawed plasma [78,79,80] (table 1).…”

Section: Trali Pathogenesis In Light Of the Innate Immune Systemmentioning

confidence: 99%

Transfusion-Related Acute Lung Injury: The Work of DAMPs*

Land¹

2013

Transfus Med Hemother

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Current notions in immunology hold that not only pathogen-mediated tissue injury but any injury activates the innate immune system. In principle, this evolutionarily highly conserved, rapid first-line defense system responds to pathogen-induced injury with the creation of infectious inflammation, and non-pathogen-induced tissue injury with ‘sterile’ tissue inflammation. In this review, evidence has been collected in support of the notion that the transfusion-related acute lung injury induces a ‘sterile’ inflammation in the lung of transfused patients in terms of an acute innate inflammatory disease. The inflammatory response is mediated by the patient’s innate immune cells including lung-passing neutrophils and pulmonary endothelial cells, which are equipped with pattern recognition receptors. These receptors are able to sense injury-induced, damage-associated molecular patterns (DAMPs) generated during collection, processing, and storage of blood/blood components. The recognition process leads to activation of these innate cells. A critical role for a protein complex known as the NLRP3 inflammasome has been suggested to be at the center of such a scenario. This complex undergoes an initial ‘priming’ step mediated by 1 class of DAMPs and then an ‘activating’ step mediated by another class of DAMPs to activate interleukin-1beta and interleukin-18. These 2 cytokines then promote, via transactivation, the formation of lung inflammation.

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“…Antiphospholipid antibodies, particularly anticardiolipin antibodies, have been associated with various neuropsychiatric manifestations [3,4,5,6]. Currently, the descriptions of epileptic seizures in patients with SLE are poorly defined.…”

Section: Introductionmentioning

confidence: 99%

Clinical Description of Seizures in Patients with Systemic Lupus Erythematosus

et al. 2008

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Objective: To evaluate the frequency of and risk factors for epileptic seizures in patients with systemic lupus erythematosus (SLE) in a large cohort series. Methods: One thousand two hundred patients with SLE were analyzed. The type and frequency of risk factors for seizures associated with SLE were studied and compared with two other series reported in the literature. Results: One hundred and forty-two patients had seizures. Seventy-five patients were studied with a mean follow-up of 5 years from the first seizure episode. Fifty-eight (77%) patients had tonic-clonic seizures, 9 (12%) complex partial seizures (PS), 5 (7%) simple partial motor seizures and 3 (4%) secondary tonic-clonic seizures. In 41 (54%) patients, the seizures occurred within the first year of the SLE diagnosis. Recurrence occurred in 40 (53%) patients, and was associated with PS in 14 (35%; p = 0.006) and time of seizures with SLE onset in 5 (12.5%; p = 0.05). Less than one third of the patients had positive antiphospholipid antibodies. A concurrent infection was present in 16 (21%) patients. Conclusions: Epileptic seizures were more common during the first year after SLE diagnosis. Neither infection nor antiphospholipid syndrome was associated with the occurrence of seizures.

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Effects of platelet release products on neutrophilic activity in human whole blood

Cited by 13 publications

References 27 publications

The apolipoprotein CIII-derived peptide, HATKTAK, and stimulation of macromolecular activators of phagocytosis from platelets (MAPPs)

The apolipoprotein CIII-derived peptide, HATKTAK, and stimulation of macromolecular activators of phagocytosis from platelets (MAPPs)

Transfusion-Related Acute Lung Injury: The Work of DAMPs*

Clinical Description of Seizures in Patients with Systemic Lupus Erythematosus

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