scholarly journals Endobronchial allergen challenge in asthma. Demonstration of cellular source of granulocyte macrophage colony-stimulating factor by in situ hybridization.

1991 ◽  
Vol 88 (3) ◽  
pp. 1048-1053 ◽  
Author(s):  
D H Broide ◽  
G S Firestein
Keyword(s):  
In Situ Hybridization ◽  
Allergen Challenge ◽  
Colony Stimulating Factor ◽  
Cellular Source ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

scholarly journals Interleukin-5 is at 5q31 and is deleted in the 5q- syndrome

Blood ◽  
1988 ◽  
Vol 71 (4) ◽  
pp. 1150-1152
Author(s):  
GR Sutherland ◽  
E Baker ◽  
DF Callen ◽  
HD Campbell ◽  
IG Young ◽  
...  
Keyword(s):  
Growth Hormone ◽  
In Situ Hybridization ◽  
Colony Stimulating Factor ◽  
Interleukin 5 ◽  
Viral Oncogene ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Viral Oncogene Homolog

Human interleukin-5 (IL-5) is a selective eosinophilopoietic and eosinophil-activating growth hormone. By in situ hybridization this gene is mapped to chromosome 5q23.3 to 5q32. It is shown to be deleted in two patients with the 5q-syndrome and in one patient previously diagnosed with myelodysplasia whose condition had progressed to acute myeloblastic leukemia. The clustering of other genes involved in hematopoiesis (IL-3, granulocyte-macrophage colony-stimulating factor, feline sarcoma viral oncogene homolog, colony-stimulating factor 1) to the same region as IL-5 suggests a nonrandom localization and raises interesting questions concerning the evolution and regulation of these genes.

scholarly journals Peripheral blood neutrophils in chronically neutropenic patients respond to granulocyte-macrophage colony-stimulating factor with a specific increase in CR1 expression and CR1 transcription

Blood ◽  
1992 ◽  
Vol 79 (7) ◽  
pp. 1667-1671 ◽  
Author(s):  
FD Jr Moore ◽  
RM Jack ◽  
JH Antin
Keyword(s):  
In Situ Hybridization ◽  
Receptor Expression ◽  
Immunofluorescent Staining ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Neutropenic Patients ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Abstract Chronically neutropenic patients from a phase I/II protocol were studied for neutrophil (PMN) abnormalities related to therapeutic use of granulocyte-macrophage colony-stimulating factor (GM-CSF). We analyzed phenotype by flow cytometry to measure indirect immunofluorescent staining and activation of transcription by in situ hybridization. PMN count increased in seven of 17 patients. For the group, PMN expression of complement receptors, CR1 and CR3, increased after GM-CSF administration (P less than .005), while expression of class 1 and FcR III was stable. PMN from both of the patients studied by in situ hybridization demonstrated increased expression of CR1 transcript, which in one case coincided in time and intensity with the course of increased CR1 expression, while in the second case the presence of CR1 mRNA increased but lagged behind the increased CR1 protein expression. Thus, PMN activation was observed after GM-CSF infusion, as indicated by increased complement receptor expression. This effect was due both to translocation of receptors from a preformed intracellular pool to the cell surface, and to transcriptional regulation leading to increased receptor synthesis.

scholarly journals Peripheral blood neutrophils in chronically neutropenic patients respond to granulocyte-macrophage colony-stimulating factor with a specific increase in CR1 expression and CR1 transcription

Blood ◽  
1992 ◽  
Vol 79 (7) ◽  
pp. 1667-1671
Author(s):  
FD Jr Moore ◽  
RM Jack ◽  
JH Antin
Keyword(s):  
In Situ Hybridization ◽  
Receptor Expression ◽  
Immunofluorescent Staining ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Neutropenic Patients ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Chronically neutropenic patients from a phase I/II protocol were studied for neutrophil (PMN) abnormalities related to therapeutic use of granulocyte-macrophage colony-stimulating factor (GM-CSF). We analyzed phenotype by flow cytometry to measure indirect immunofluorescent staining and activation of transcription by in situ hybridization. PMN count increased in seven of 17 patients. For the group, PMN expression of complement receptors, CR1 and CR3, increased after GM-CSF administration (P less than .005), while expression of class 1 and FcR III was stable. PMN from both of the patients studied by in situ hybridization demonstrated increased expression of CR1 transcript, which in one case coincided in time and intensity with the course of increased CR1 expression, while in the second case the presence of CR1 mRNA increased but lagged behind the increased CR1 protein expression. Thus, PMN activation was observed after GM-CSF infusion, as indicated by increased complement receptor expression. This effect was due both to translocation of receptors from a preformed intracellular pool to the cell surface, and to transcriptional regulation leading to increased receptor synthesis.

scholarly journals Interleukin-5 is at 5q31 and is deleted in the 5q- syndrome

Blood ◽  
1988 ◽  
Vol 71 (4) ◽  
pp. 1150-1152 ◽  
Author(s):  
GR Sutherland ◽  
E Baker ◽  
DF Callen ◽  
HD Campbell ◽  
IG Young ◽  
...  
Keyword(s):  
Growth Hormone ◽  
In Situ Hybridization ◽  
Colony Stimulating Factor ◽  
Interleukin 5 ◽  
Viral Oncogene ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor ◽  
Viral Oncogene Homolog

Abstract Human interleukin-5 (IL-5) is a selective eosinophilopoietic and eosinophil-activating growth hormone. By in situ hybridization this gene is mapped to chromosome 5q23.3 to 5q32. It is shown to be deleted in two patients with the 5q-syndrome and in one patient previously diagnosed with myelodysplasia whose condition had progressed to acute myeloblastic leukemia. The clustering of other genes involved in hematopoiesis (IL-3, granulocyte-macrophage colony-stimulating factor, feline sarcoma viral oncogene homolog, colony-stimulating factor 1) to the same region as IL-5 suggests a nonrandom localization and raises interesting questions concerning the evolution and regulation of these genes.

scholarly journals Cytokine expression in allergic inflammation: systematic review ofin vivochallenge studies

2003 ◽  
Vol 12 (5) ◽  
pp. 259-267 ◽  
Author(s):  
Manuel A. R. Ferreira
Keyword(s):  
Inflammatory Responses ◽  
Allergic Inflammation ◽  
Allergen Challenge ◽  
Cytokine Expression ◽  
Colony Stimulating Factor ◽  
Control Value ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Stimulating Factor

Background:Allergic inflammatory responses are driven by cells of the immune system that rely on cytokines to regulate the activity of other immune and structural cells.Objective:To review published studies to (1) identify cytokines consistently increased after allergen challenge in atopic patients and (2) investigate temporal variation in cytokine expression.Methods:A PUBMED systematic search was used to extract data from studies involving analysis of cytokine expression in fluids or biopsies followingin vivoallergen challenge in atopic patients.Results:Data were extracted from 82 studies. There were no consistent reports of cytokine protein increase in fluids of patients at 0-1 h after challenge. At 4-12 h, the chemokines eotaxin, macrophage inflammatory protein-1α, RANTES (regulated on activation normal T cell expressed and secreted) and interleukin (IL)-8 have all been consistently reported to be up-regulated. At 18-24 h after challenge, the lymphokines IL-4, IL-5 and IL-13, as well as the pro-inflammatory cytokines granulocyte-macrophage colony-stimulating factor, tumour necrosis factor-α and IL-6 are consistently increased when compared with the respective control value. There were no reports of up-regulation in interferon-γprotein and mRNA and in IL-2 mRNA.Conclusion:The expression of granulocyte-macrophage colony-stimulating factor is consistently increased in tissues at 4-12 h after challenge. The influence of this cytokine on antigen capture and presentation by dendritic cells should be further investigated. Additionally, allergen challenge studies are needed that investigate the expression of macrophage-derived chemokine and thymus-regulated and activation-regulated chemokine in tissues of atopic patients. Blocking the effects of these lymphocyte-specific chemokines might provide new therapeutic approaches for the control of allergic inflammation.

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