Immunohistochemical detection of GM-CSF, IL-4 and IL-5 in a murine model of allergic bronchopulmonary aspergillosis

1996 ◽  
Vol 26 (4) ◽  
pp. 461-468 ◽  
Author(s):  
H. W. CHU ◽  
J. M. WANG ◽  
M. BOUTET ◽  
L. P. BOULET ◽  
M. LAVIOLETTE
Keyword(s):  
Murine Model ◽  
Allergic Bronchopulmonary Aspergillosis ◽  
Immunohistochemical Detection ◽  
Gm Csf

scholarly journals Second-Hand Smoke Increases Bronchial Hyperreactivity and Eosinophilia in a Murine Model of Allergic Aspergillosis

2003 ◽  
Vol 10 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Brian W. P. Seymour ◽  
Edward S. Schelegle ◽  
Kent E. Pinkerton ◽  
Kathleen E. Friebertshauser ◽  
Janice L. Peake ◽  
...  
Keyword(s):  
Tobacco Smoke ◽  
Murine Model ◽  
Airway Hyperresponsiveness ◽  
Allergic Bronchopulmonary Aspergillosis ◽  
Ambient Air ◽  
Airway Hyperreactivity ◽  
Second Hand Smoke ◽  
Th2 Response ◽  
Allergic Lung Disease ◽  
Public Areas

Involuntary inhalation of tobacco smoke has been shown to aggravate the allergic response. Antibodies to fungal antigens such asAspergillus fumigatus(Af) cause an allergic lung disease in humans. This study was carried out to determine the effect of environmental tobacco smoke (ETS) on a murine model of allergic bronchopulmonary aspergillosis (ABPA). BALB/c mice were exposed to aged and diluted sidestream cigarette smoke to simulate 'second-hand smoke'. The concentration was consistent with that achieved in enclosed public areas or households where multiple people smoke. During exposure, mice were sensitized to Af antigen intranasally. Mice that were sensitized to Af antigen and exposed to ETS developed significantly greater airway hyperreactivity than did mice similarly sensitized to Af but housed in ambient air. The effective concentration of aerosolized acetylcholine needed to double pulmonary flow resistance was significantly lower in Af + ETS mice compared to the Af + AIR mice. Immunological data that supports this exacerbation of airway hyperresponsiveness being mediated by an enhanced type 1 hypersensitivity response include: eosinophilia in peripheral blood and lung sections. All Af sensitized mice produced elevated levels of IL4, IL5 and IL10 but no IFN-γ indicating a polarized Th2 response. Thus, ETS can cause exacerbation of asthma in ABPA as demonstrated by functional airway hyperresponsiveness and elevated levels of blood eosinophilia.

scholarly journals Bead-Selected Antitumor Genetic Cell Vaccines

2008 ◽  
Vol 2 ◽  
pp. CMO.S586
Author(s):  
Herrero Mj ◽  
R Botella ◽  
R Algás ◽  
FM Marco ◽  
Aliño Sf
Keyword(s):  
Gene Therapy ◽  
Immune Response ◽  
Tumor Cells ◽  
Murine Model ◽  
Cancer Vaccines ◽  
Genetically Modified ◽  
Cell Number ◽  
Gm Csf ◽  
Clinical Reality

Cancer vaccines have always been in the scope of gene therapy research. One of the most successful approaches has been working with genetically modified tumor cells. However, to become a clinical reality, tumor cells must suffer a long and risky process from the extraction from the patient to the reimplantation as a vaccine. In this work, we explain our group's approach to reduce the cell number required to achieve an immune response against a melanoma murine model, employing bead-selected B16 tumor cells expressing GM-CSF and B7.2.

IRF-4 Functions as a Myeloid Tumor Suppressor.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 2206-2206
Author(s):  
Jaime Acquaviva ◽  
Jonathan Schatz ◽  
Harinder Singh ◽  
Ruibao Ren
Keyword(s):  
Tumor Suppressor ◽  
Progenitor Cells ◽  
Murine Model ◽  
Cell System ◽  
Myelogenous Leukemia ◽  
Myeloproliferative Disease ◽  
Granulocytic Differentiation ◽  
Gm Csf ◽  
Myeloid Progenitor Cells ◽  
Colony Forming Capacity

Abstract Interferon regulatory factor 4 (IRF-4, also know as pip, LSIRF, ICSAT and MUM1) is a transcription factor with well-characterized functions in B and T cell development and immune response regulation. Though its expression has been demonstrated in macrophages, its function in the myeloid system is not as well characterized. The closely related IRF family member IRF-8 (ICSBP) has more clearly defined functions in the myeloid system. IRF-8 is a critical regulator of myelopoiesis, and its loss has been implicated in the pathogenesis of chronic myelogenous leukemia (CML). IRF-8 deficient mice manifest a CML-like syndrome, and we have shown previously that forced expression of IRF-8 in a BCR/ABL-induced murine model of CML represses the resulting myeloproliferative disease and prolongs survival. In the B-cell system, we have found that IRF-4 and IRF-8 function redundantly at the pre-B-to-B transition point of development. In this study we investigate whether IRF-4 and IRF-8 may also have overlapping function in myeloid cells. Our results show that mice deficient in both IRF-4 and IRF-8 develop from a very early age a more aggressive CML-like disease than mice deficient in IRF-8 alone. Bone marrow progenitors from IRF-4/8 DKO mice have increased proliferation, GM-CSF stimulated granulocytic differentiation, and colony-forming capacity compared to progenitors from WT or single KO mice. These data suggest that IRF-4 plays a role in myeloid lineage development and may act to suppress proliferation and granulocytic differentiation of myeloid progenitor cells. We further examined if, like IRF-8, IRF-4 is able to suppress BCR/ABL mediated transformation. We used a murine stem cell virus vector to co-express BCR/ABL and either IRF-4 or IRF-8 in BM progenitor cells and assessed colony forming capacity of infected cultures as well as the ability of IRF-4 to suppress BCR/ABL induced CML-like disease in a murine model. Our results demonstrate that IRF-4 potently suppresses BCR/ABL induced colony formation and that forced expression of IRF-4 suppresses BCR/ABL-induced CML-like disease in mice even more potently than IRF-8. These results provide direct evidence that IRF-4 is an important myeloid tumor suppressor and may allow elucidation of new molecular pathways significant to the pathogenesis of human CML.

scholarly journals Second-hand Smoke Increases Nitric Oxide and Alters the IgE Response in a Murine Model of Allergic Aspergillosis

2005 ◽  
Vol 12 (2) ◽  
pp. 113-124 ◽  
Author(s):  
Brian W. P. Seymour ◽  
Janice L. Peake ◽  
Kent E. Pinkerton ◽  
Viswanath P. Kurup ◽  
Laurel J. Gershwin
Keyword(s):  
Nitric Oxide ◽  
Murine Model ◽  
Allergic Bronchopulmonary Aspergillosis ◽  
Ambient Air ◽  
Lung Parenchyma ◽  
Second Hand Smoke ◽  
No Production ◽  
Ifn Γ ◽  
Ige Response

This study was performed to determine the effects of environmental tobacco smoke (ETS) on nitric oxide (NO) and immunoglobulin (Ig) production in a murine model of allergic bronchopulmonary aspergillosis (ABPA). Adult BALB/c mice were exposed to aged and diluted sidestream cigarette smoke from day 0 through day 43 to simulate “second-hand smoke”. During exposure, mice were sensitized to solubleAspergillus fumigatus(Af) antigen intranasally between day 14 and 24. All Af sensitized mice in ambient air (Af + AIR) made elevated levels of IgE, IgG1, IgM, IgG2a and IgA. Af sensitized mice housed in ETS (Af + ETS) made similar levels of immunoglobulins except for IgE that was significantly reduced in the serum and bronchoalveolar lavage (BAL). However, immunohistochemical evaluation of the lung revealed a marked accumulation of IgE positive cells in the lung parenchyma of these Af + ETS mice. LPS stimulation of BAL cells revealed elevated levels of NO in the Af + AIR group, which was further enhanced in the Af+ETS group.In vitrorestimulation of the BAL cells on day 45 showed a TH0 response with elevated levels of IL3, 4, 5, 10 and IFN-γ. However, by day 28 the response shifted such that TH2 cytokines increased while IFN-γ decreased. The Af + ETS group showed markedly reduced levels in all cytokines tested, including the inflammatory cytokine IL6, when compared to the Af+AIR group. These results demonstrate that ETS affects ABPA by further enhancing the NO production and reduces the TH2 and the inflammatory cytokines while altering the pattern of IgE responses.

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