scholarly journals Neutrophil activation in vitro and in vivo in Wegener's granulomatosis

1994 ◽  
Vol 45 (4) ◽  
pp. 1120-1131 ◽  
Author(s):  
Elisabeth Brouwer ◽  
Minke G. Huitema ◽  
A.H. Leontine Mulder ◽  
Peter Heeringa ◽  
Harry van Goor ◽  
...  
1987 ◽  
Author(s):  
L Chrobák ◽  
V Rozsíval ◽  
V Herout

In a 23-year-old man with Wegener’s granulomatosis and mild bleeding coagulation studies revealed a significant prolongation of the coagulation time (CT) prothrombin time (PT), activated partial thromboplastin time (aPTT), thrombin time (TT), failure of TT and aPTT to correct in a 1:1 mixture with pooled normal plasma (PNP), correction of the prolonged TT with toluidine blue and correction of TT and aPTT both in vitro and in vivo^protamine sulphate (P.S.).All other coagulation tests, i.e.,bleeding time, platelet count? fibrinogen level, euglobulme lysis time were within normal limits. The patient did not receive heparine. TT after administration of 5ml of protamine sulphate i.v. to the patient became normal - 18,2 s (19,7 s).In summary a patient with Wegener s granulomatosis associated with an endogenous heparine-like anticoagulant is reported. The anticoagulant could be corrected both in vitro and in vivo by protamine sulphate.


2005 ◽  
Vol 146 (3) ◽  
pp. 344-351 ◽  
Author(s):  
Bruce D Levy ◽  
Lorraine Hickey ◽  
Andrew J Morris ◽  
Mykol Larvie ◽  
Raquel Keledjian ◽  
...  

2017 ◽  
Vol 1 (11) ◽  
pp. 662-668 ◽  
Author(s):  
Yuyan Shen ◽  
Hong Hong ◽  
Panjamaporn Sangwung ◽  
Stephanie Lapping ◽  
Lalitha Nayak ◽  
...  

Key Points KLF4 deficiency impairs neutrophil function in vitro and in vivo. This is the first demonstration that KLF4 plays a crucial role in neutrophils.


2010 ◽  
Vol 361 (1-2) ◽  
pp. 82-88 ◽  
Author(s):  
Josefin M. Paulsson ◽  
Stefan H. Jacobson ◽  
Joachim Lundahl

1987 ◽  
Author(s):  
C Alessandri ◽  
F Violi ◽  
M Rasura ◽  
C Caliendo ◽  
P Pelaia

Histopathological studies in segments of cerebral ischaemia show local inflammation with leucocytes infiltration.This event has been confirmed in vivo by means of radiolabelled leucocytes. This inflammatory response could be of detriment to cerebral tissue since leucocytes release toxic substances such as oxygen free radicals.A free radical mechanism,in fact,has been supposed as an event worsening the evolution of ischemia.Evidence of neutrophil activation in stroke patients was shown by us in previous reports, where we have described that the plasma of these patients contained an excess of a neutrophil oxidase able to convert,in vitro, adrenaline to adrenochrome.Aim of present study was to evaluate if neutrophil activation can be observed in patients with brain hemor ragie (BH) also.Six patients (females 1,males 5;age 68-79 years) suffering from BH and 15 patients (females 5, Males 10;age 58-86 years) affected by brain infarction (BI) were studied within 20-48 hours from acute episode.Diagnosis of stroke was made by computerized tomography.Neutrophil activation was studied in plasma evaluating the oxidation of adrenaline to adrenochrome according to Matthews and Campbell method.20 matched for age and sex healthy subjects were studied as control.A significant rise of plasma adrenaline oxidase activity was observed in patients with BI.This preliminary investigation suggests that neutrophil activation could be restricted to patients with BI.In fact,patients with BH had plasma oxidase activity similar to controls.Clinical data should be necessary to evaluate if a relation between leucocyte activation and the natural course of cerebral ischemia does exist.


2021 ◽  
Author(s):  
Peter Rosenberger ◽  
Tiago Granja

Pulmonary defense mechanisms are critical for host integrity during the early phase of pneumonia and sepsis. These processes are fundamentally dependent on the activation of neutrophils during the early phase of the innate immune response. Recent work has shown that semaphorin 7A (Sema7A) holds significant impact on platelet activation, yet its role in neutrophil migration and function is not well known. We report here that Sema7A binds to neutrophil PlexinC1, increasing integrins and L-selectin on the neutrophil surface. Sema7A-induced neutrophil activation also prompted neutrophil chemotaxis in vitro and the formation of platelet-neutrophil complexes in vivo. We also observed altered adhesion and transmigration of neutrophils in Sema7A-/- animals in the lung. Sema7A-/- animals also showed altered crawling properties of neutrophils. This resulted in increased number of neutrophils in the interstitial space of Sema7A-/- animals but reduced numbers of neutrophils in the alveolar space during pneumonia-induced pulmonary sepsis. This was associated with significantly worse outcome of Sema7A-/- animals in a model of Klebsiella pneumoniae. Furthermore, we were able to show a correlation between serum levels of Sema7A in patients with ARDS and oxygenation levels. Thus, we show here that Sema7A has an immunomodulatory effect though which might influence patient outcome during pulmonary sepsis.


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