scholarly journals What can we learn from blood granulocyte patterns in patients with asthma?

2016 ◽  
Vol 48 (4) ◽  
pp. 976-978 ◽  
Author(s):  
Kirsty Hambleton ◽  
Ian D. Pavord
Keyword(s):  
2021 ◽  
pp. 194589242199303
Author(s):  
Lihong Wang ◽  
Mengmeng Zhan ◽  
Junling Wang ◽  
Dong Chen ◽  
Nan Zhao ◽  
...  

Background Recently, it has been reported that Toll-like receptor 7 (TLR7) agonists can improve allergic rhinitis (AR) symptoms by up-regulation of Th1 cytokine release and suppression of Th2 cell functions. However, little is known of the expression of TLR7 in basophils of AR. Objective To explore the expression of TLR7 in basophils of AR, and influence of allergens on TLR7 expression. Methods The expression levels of TLR7 in basophils of patients with AR were determined by flow cytometry, and the influence of allergens on TLR7 expression was examined by real time (q) PCR. Results The percentages of TLR7+CCR3+ cells ( P < 0.001 and P = 0.011), TLR7+CD123+HLA-DR− cells ( P = 0 .016 and P = 0.042) and TLR7+CCR3+CD123+HLA-DR− cells ( P = 0.046 and P = 0.035) in blood granulocyte and mononucleated cell populations of the patients with AR were increased, respectively compared with HC subjects. TLR7 MFI on CCR3+ cells ( P = 0.050 and P = 0.043), CD123+HLA-DR− cells ( P < 0.001 and P = 0.002) and CCR3+CD123+HLA-DR− cells ( P < 0.001 and P = 0.003) were enhanced compared with HC subjects. Allergens Der p1 and OVA provoked upregulation of TLR7 expression at both protein and mRNA levels and IL-13 production in KU812 cells. House Dust Mite extract (HDME), Artemisia sieversiana wild allergen extract (ASWE), IL-31, IL-33, IL-37, and TSLP provoked elevation of IL-6 release from KU812 cells following 2 h incubation period. Conclusions The percentage of TLR7+ basophils and TLR7 expression intensity in a single basophil are both increased in the blood of patients with AR, indicating that basophils likely contribute to the pathogenesis of AR via TLR7.


Allergy ◽  
2017 ◽  
Vol 72 (8) ◽  
pp. 1202-1211 ◽  
Author(s):  
B. Hilvering ◽  
S. J. H. Vijverberg ◽  
J. Jansen ◽  
L. Houben ◽  
R. C. Schweizer ◽  
...  

2007 ◽  
Vol 564 (1-3) ◽  
pp. 146-149 ◽  
Author(s):  
Jaouad Bouayed ◽  
Hassan Rammal ◽  
Chafique Younos ◽  
Rachid Soulimani

1986 ◽  
Vol 4 (3) ◽  
pp. 318-324 ◽  
Author(s):  
L Tschopp ◽  
V E von Fliedner ◽  
C Sauter ◽  
P Maurice ◽  
A Gratwohl ◽  
...  

We investigated the tolerance, efficacy, and clinical cross-resistance of a new combination chemotherapy in 38 patients with previously treated acute myeloblastic leukemia (AML). It consisted of 120 mg2/d 4'(9-acridinylamino) methanesulfon-m-Anisidide (m-AMSA) in a one-hour infusion and 80 mg/m2/d etoposide (VP-16) in a 24-hour infusion, both administered for 5 days. The first 27 patients also received vinblastine, 6 mg/m2 on day 8, but this therapy was discontinued because of intestinal complications. Thirteen of 23 patients (56%) at first or subsequent relapse and five of 15 patients (33%) who were primarily resistant to an anthracycline/cytarabine combination achieved a complete response (CR) (hemoglobin level not taken into account) with a median CR duration of 5 months and 2 months, respectively. The response rate was as high as 63% for patients at first or second relapse whether the remission was maintained or not. The median times to recovery of normal bone marrow cellularity, of blood granulocyte counts greater than 500/microL, and of platelets greater than 20,000/microL were 34, 27, and 22 days, respectively. Marked but reversible gastrointestinal toxicity was observed in 24% of the patients, and two patients died of infection during induction. The one-hour AMSA/continuous VP-16 combination is effective for patients with relapsing AML and shows no cross-resistance in a proportion of patients refractory to the standard anthracycline-cytarabine combination.


Blood ◽  
1974 ◽  
Vol 43 (5) ◽  
pp. 645-656 ◽  
Author(s):  
Rosa T. Canoso ◽  
Robert Rodvien ◽  
Kristine Scoon ◽  
Peter H. Levine

Abstract Hydrogen peroxide, at concentrations in the micromolar range, can influence platelet function. Although H2O2 causes no detectable platelet aggregation at these concentrations, it can aggregate platelets which have been previously exposed to any of several aggregating agents. H2O2 can enhance bath aggregation and the subsequent disaggregation of platelets, as initiated by ADP. Preexposure of platelets to H2O2 blunts the subsequent response to ADP. Washed platelets are susceptible to H2O2. Catalase-treated H2O2 has no effect on platelet function. H2O2 does not appear to act by altering either the aggregating agent or plasma thrombin generation. These data suggest that minute amounts of H2O2, which could theoretically be generated in vivo at sites of platelet plug formation, could play a regulatory role in the dynamics of growth and/or dissipation of the hemostatic plug. The blood granulocyte could participate in hemostasis and thrombosis via H2O2 generation.


1967 ◽  
Vol 17 (1) ◽  
pp. 18-29
Author(s):  
A. Fieschi ◽  
C. Sacchetti

SummarySelected subjects have been treated with cyclophosphamide and nitrogen mustard. The granulocytopenia has been followed by repeated in vivo labeling with DFP32 and the endotoxin test for evaluating the availability of the granulocyte reserve. The effect of steroid treatment on the recovery of the granulopoiesis has been studied with autotransfusions of in vitro DFP32 labeled granulocytes in the same subject and performed before, during and after the treatment was discontinued.The following conclusions have been reached:1. The efficiency of the granulopoiesis is based upon the availability of the bone marrow granulocyte reserve.2. The bone marrow granulocyte mobilization with endotoxin and the in vivo granulocyte labeling with DFP32 give an evaluable information about the bone marrow granulocyte reserve.3. The granulocytopenia due to antiblastic therapy corresponds to a depletion of the bone marrow granulocyte reserve.4. The recovery of a “normal granulocyte count” preceeds the rebuilt of a “normal availability” of the bone marrow granulocyte reserve.5. The recovery of the blood granulocyte count after prednison is not associated with any favourable change of the granulopoiesis.


1964 ◽  
Vol 206 (1) ◽  
pp. 83-88 ◽  
Author(s):  
S. O. Raab ◽  
J. W. Athens ◽  
O. P. Haab ◽  
D. R. Boggs ◽  
H. Ashenbrucker ◽  
...  

Dog granulocytes were labeled in vitro with radioactive diisopropylfluorophosphate (DFP32) and then returned to the circulation of the donor. Granulocytes were separated from whole blood by utilizing hexadimethrine bromide as the sedimenting agent and saponin as a lysing agent. The labeled granulocytes disappeared from the circulation in an exponential fashion with a mean (±1 sd) half-time disappearance of 5.6 ± 0.95 hr. The size of the total blood granulocyte ( TBGP), circulating granulocyte ( CGP), and marginal granulocyte ( MGP) pools, and the granulocyte turnover rate ( GTR) were measured in 31 normal, unanesthetized dogs. The mean values ± 1 sd, expressed as number of cells x107/kg body wt., were as follows: TBGP, 102 ± 34.8; CGP, 54 ± 20.7; MGP, 48 ± 23.4; and GTR, 305 ± 111.5 cells/kg day. The values observed in anesthetized and in unanesthetized, splenectomized dogs were not significantly different from the above values.


The Lancet ◽  
1973 ◽  
Vol 301 (7793) ◽  
pp. 37-38 ◽  
Author(s):  
J Hakim ◽  
P Boivin ◽  
J Boucherot ◽  
H Troube

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