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Granulocyte_Macrophage Colony Stimulating Factor (GM_CSF), Clone CC305, Mab anti_Bovine; ELISA_WB

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[#YSRTMCA1828] Granulocyte_Macrophage Colony Stimulating Factor (GM_CSF), Clone CC305, Mab anti_Bovine; ELISA_WB

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YSRTMCA1828 | Granulocyte_Macrophage Colony Stimulating Factor (GM_CSF), Clone CC305, Mab anti_Bovine; ELISA_WB, 0.5 mg.
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(1) Granulocyte-Macrophage Colony-Stimulating Factor as a Therapeutic Target in Multiple Sclerosis.[TOP]

Pubmed ID :30506485
Publication Date : //
Multiple sclerosis is an inflammatory neurodegenerative disease of the central nervous system (CNS) and the most frequent cause of non-traumatic disability in adults in the Western world. Currently, several drugs have been approved for the treatment of multiple sclerosis. While the newer drugs are more effective, they have less favourable safety profiles. Thus, there is a need to identify new targets for effective and safe therapies, particularly in patients with progressive disease for whom no treatments are available. One such target is granulocyte-macrophage colony-stimulating factor (GM-CSF) or its receptor. In this article we review data on the potential role of GM-CSF and GM-CSF inhibition in MS. We discuss the expression and function of GM-CSF and its receptor in the CNS, as well as data from animal studies and clinical trials in MS.

Authors : Aram Jehan, Francis Anna, Tanasescu Radu, Constantinescu Cris S,



(2) Management of a Patient With Congenital Biallelic CSF3R Mutation With GM-CSF.[TOP]

Pubmed ID :30499904
Publication Date : //
Severe Congenital Neutropenia (SCN) is a rare inherited disease characterized by an absolute neutrophil count (ANC) lower than 500/μL. Genetic heterogeneity and biallelic CSF3R mutation has rarely been identified as an underlying genetic defect in SCN. The majority of SCN patients respond to granulocyte colony stimulating factor treatment; however, in patients with inherited CSF3R mutation, ANC cannot generally be increased with granulocyte colony stimulating factor treatment. In such cases, granulocyte macrophage colony stimulating factor presents as an effective treatment option. Herein, we report a case of a 5-year-old SCN girl with homozygous c610-611 del ins AG (p.Q204R) mutation in the CSF3R gene, who was successfully treated with granulocyte macrophage colony stimulating factor.

Authors : Yilmaz Karapinar Deniz, Özdemir Hamiyet Hekimci, Akinci Burcu, Yaşar Akkiz Şahin, Siviş Zuhal Önder, Onay Hüseyin, Özkinay Ferda,



(3) Graft-versus-host disease, but not graft-versus-leukemia immunity, is mediated by GM-CSF-licensed myeloid cells.[TOP]

Pubmed ID :30487251
Publication Date : //
Allogeneic hematopoietic cell transplantation (allo-HCT) not only is an effective treatment for several hematologic malignancies but can also result in potentially life-threatening graft-versus-host disease (GvHD). GvHD is caused by T cells within the allograft attacking nonmalignant host tissues; however, these same T cells mediate the therapeutic graft-versus-leukemia (GvL) response. Thus, there is an urgent need to understand how to mechanistically uncouple GvL from GvHD. Using preclinical models of full and partial MHC-mismatched HCT, we here show that the granulocyte-macrophage colony-stimulating factor (GM-CSF) produced by allogeneic T cells distinguishes between the two processes. GM-CSF drives GvHD pathology by licensing donor-derived phagocytes to produce inflammatory mediators such as interleukin-1β and reactive oxygen species. In contrast, GM-CSF did not affect allogeneic T cells or their capacity to eliminate leukemic cells, retaining undiminished GvL responses. Last, tissue biopsies and peripheral blood mononuclear cells from patients with grade IV GvHD showed an elevation of GM-CSF-producing T cells, suggesting that GM-CSF neutralization has translational potential in allo-HCT.

Authors : Tugues Sonia, Amorim Ana, Spath Sabine, Martin-Blondel Guillaume, Schreiner Bettina, De Feo Donatella, Lutz Mirjam, Guscetti Franco, Apostolova Petya, Haftmann Claudia, Hasselblatt Peter, Núñez Nicolas G, Hottiger Michael O, van den Broek Maries, Manz Markus G, Zeiser Robert, Becher Burkhard,



(4) Incense Smoke Exposure Augments Systemic Oxidative Stress, Inflammation and Endothelial Dysfunction in Male Albino Rats.[TOP]

Pubmed ID :30480468
Publication Date : //
Incense smoke is reported to increase cardiovascular disease (CVD) risk in exposed individuals. However, the mechanism underlying the toxic effect of incense smoke on cardiovascular system is unclear. To test this, we chronically exposed male albino rats to two different types of Arabian incense smoke and studied their effects on oxidative stress, inflammation and endothelial function. Rats exposed to either of incense smoke showed a significant increase in malondialdehyde (MDA) and a significant decline in superoxide dismutase (SOD) and reduced glutathione (GSH). Endothelial functional marker, nitric oxide (NO) was significantly decreased while endothelin-1 was significantly increased in rats exposed to both the incense types. Incense smoke exposure also led to a significant increase in chemokines and inflammatory mediators including monocyte chemoattractant protein-1 (MCP-1), granulocyte-macrophage-colony stimulating factor (GM-CSF), regulated on activation normal T cell expressed and secreted (RANTES), interleukin-4 (IL-4), C-reactive protein (CRP), and tumor necrosis factor-alpha (TNF-α). Besides, incense smoke exposed rats demonstrated a significant increase in the expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecules-1 (VCAM-1), and E-selectin. Importantly, cessation of incense smoke exposure for 30 days led to a significant reversal in the levels of all the studied markers. Collectively, this study describes oxidative stress, endothelial dysfunction and inflammation as possible underlying mechanisms in the toxic effects of incense smoke on increased CVD risk in incense smoke exposed individuals. Findings also underscore that the avoiding incense smoke exposure may have beneficial health effects.

Authors : Hussain Tajamul, Alamery Salman, Gambhir Dikshit, Mohammed Arif A, Naushad Shaik M, Alrokayan Salman,



(5) Increased expression of L-plastin in nasal polyp of patients with nonsteroidal anti-inflammatory drug exacerbated respiratory disease.[TOP]

Pubmed ID :30479022
Publication Date : //
Most patients with nonsteroidal anti-inflammatory drug exacerbated respiratory disease (NERD) suffer from recurrence of nasal polyps. However, little is known about the specific cellular and molecular mechanisms contributing to the pathogenesis of nasal polyp development in patients with NERD in particular, especially at baseline when cyclooxygenase 1 inhibitors are not present. The objectives of this study were to identify proteins involved in the pathogenesis of nasal polyps in patients with NERD.

Authors : Takabayashi Tetsuji, Tanaka Yukie, Susuki Dai, Yoshida Kanako, Tomita Kaori, Sakashita Masafumi, Imoto Yoshimasa, Kato Yukinori, Narita Norihiko, Nakayama Tsugihisa, Haruna Shinichi, Schleimer Robert P, Fujieda Shigeharu,



(6) Graphene quantum dots inhibit T cell-mediated neuroinflammation in rats.[TOP]

Pubmed ID :30471296
Publication Date : //
We investigated the therapeutic capacity of nano-sized graphene sheets, called graphene quantum dots (GQD), in experimental autoimmune encephalomyelitis (EAE), an animal model of immune-mediated central nervous system (CNS) damage. Intraperitoneally administered GQD (10 mg/kg/day) accumulated in the lymph node and CNS cells of Dark Agouti rats in which EAE was induced by immunization with spinal cord homogenate in complete Freund's adjuvant. GQD significantly reduced clinical signs of EAE when applied throughout the course of the disease (day 0-32), while the protection was less pronounced if the treatment was limited to the induction (day 0-7 post-immunization) or effector (from day 8 onwards) phase of the disease. GQD treatment diminished immune infiltration, demyelination, axonal damage, and apoptotic death in the CNS of EAE animals. GQD also reduced the numbers of interferon-γ-expressing T helper (Th)1 cells, as well as the expression of Th1 transcription factor T-bet and proinflammatory cytokines tumor necrosis factor, interleukin-1, and granulocyte-macrophage colony-stimulating factor in the lymph nodes and CNS immune infitrates. The protective effect of GQD in EAE was associated with the activation of p38 and p42/44 mitogen-activated protein kinases (MAPK) and Akt in the lymph nodes and/or CNS. Finally, GQD protected oligodendrocytes and neurons from T cell-mediated damage in the in vitro conditions. Collectively, these data demonstrate the ability of GQD to gain access to both immune and CNS cells during neuroinflammation, and to alleviate immune-mediated CNS damage by modulating MAPK/Akt signaling and encephalitogenic Th1 immune response.

Authors : Tosic Jelena, Stanojevic Zeljka, Vidicevic Sasenka, Isakovic Aleksandra, Ciric Darko, Martinovic Tamara, Kravic-Stevovic Tamara, Bumbasirevic Vladimir, Paunovic Verica, Jovanovic Svetlana, Todorovic-Markovic Biljana, Markovic Zoran, Danko Martin, Micusik Matej, Spitalsky Zdenko, Trajkovic Vladimir,



(7) GM-CSF inhibition reduces cytokine release syndrome and neuroinflammation but enhances CAR-T cell function in xenografts.[TOP]

Pubmed ID :30463995
Publication Date : //
Chimeric antigen receptor T (CAR-T) cell therapy is a new pillar in cancer therapeutics; however, its application is limited by the associated toxicities. These include cytokine release syndrome (CRS) and neurotoxicity. While the IL-6R antagonist tocilizumab is approved for treatment of CRS, there is no approved treatment of neurotoxicity associated with CD19 targeted CAR-T (CART19) cell therapy. Recent data suggest that monocytes and macrophages contribute to the development of CRS and neurotoxicity after CAR-T cell therapy. Therefore, we investigated neutralizing granulocyte macrophage colony-stimulating factor (GM-CSF) as a potential strategy to manage CART19 cell associated toxicities. In this study, we show that GM-CSF neutralization with lenzilumab does not inhibit CART19 function in vitro or in vivo. Moreover, CART19 cell proliferation was enhanced and durable control of leukemic disease was maintained better in patient derived xenografts after GM-CSF neutralization with lenzilumab. In a primary acute lymphoblastic leukemia (ALL) xenograft model of CRS and neuro-inflammation (NI), GM-CSF neutralization resulted in a reduction of myeloid and T cell infiltration in the central nervous system and a significant reduction in NI and prevention of CRS. Finally, we generated GM-CSF deficient CART19 cells through CRISPR/Cas9 disruption of GM-CSF during CAR-T cell manufacturing. These GM-CSF CAR-T cells maintained normal functions, had enhanced anti-tumor activity in vivo, and improved overall survival compared to CART19. Together, these studies illuminate a novel approach to abrogate NI and CRS through GM-CSF neutralization, which may potentially enhance CAR-T cell function. Phase II studies with lenzilumab in combination with CART19 therapy are planned.

Authors : Sterner Rosalie M, Sakemura Reona, Cox Michelle J, Yang Nan, Khadka Roman H, Forsman Cynthia L, Hansen Michael J, Jin Fang, Ayasoufi Katayoun, Hefazi Mehrdad, Schick Kendall J, Walters Denise K, Ahmed Omar, Chappell Dale, Sahmoud Tarek, Durrant Cameron, Nevala Wendy K, Patnaik Mrinal M, Pease Larry, Hedin Karen E, Kay Neil E, Johnson Aaron J, Kenderian Saad S,



(8) Interleukin-12 as a biomarker of the beneficial effects of food restriction in mice receiving high fat diet or high carbohydrate diet.[TOP]

Pubmed ID :30462775
Publication Date : //
The impact of food restriction (FR) during 56 days on serum levels of cytokines in mice fed a high-fat diet (HFD) or high-carbohydrate diet (HCD) were evaluated. The amount of food was reduced 50% for HFD-FR and HCD-FR groups compared to mice receiving free access to HFD (HFD group) or HCD (HCD group). We quantified the serum levels of basic fibroblast growth factor, granulocyte-macrophage colony-stimulating factor, inducible protein 10, interferon γ, interleukin 1α (IL-1α), IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-12, IL-13, IL-17, keratinocyte chemoattractant, macrophage inflammatory protein-1α, monocyte chemotactic protein 1, monokine induced by IFN-γ, and tumor necrosis factor α. Only IL-12 levels were lower (P<0.05), for both HFD-FR (HFD-FR vs HFD) and HCD-FR (HCD-FR vs HCD). Therefore, IL-12 levels could be considered a biological marker of the beneficial effects of FR.

Authors : de Almeida-Souza C B, Antunes M M, Godoy G, Schamber C R, Silva M A R C P, Bazotte R B,



(9) Autoimmune pulmonary alveolar proteinosis presenting peripheral ground-glass opacities.[TOP]

Pubmed ID :30459948
Publication Date : //
Autoimmune pulmonary alveolar proteinosis should be considered in the differential diagnosis of peripheral ground-glass opacities.

Authors : Sugino Keishi, Ando Masahiro, Mori Kiyoshi, Tsuboi Eiyasu,



(10) GM-CSF therapy inhibits chronic graft-versus-host disease via expansion of regulatory T cells.[TOP]

Pubmed ID :30457669
Publication Date : //
Regulatory T cells (Tregs) attenuate excessive immune responses, making their expansion beneficial in immune-mediated diseases, including allogeneic bone marrow transplantation associated with graft-versus-host disease (GVHD). In addition to interleukin-2, Tregs require T-cell receptor and costimulatory signals from antigen-presenting cells, such as DCs, for their optimal proliferation. Granulocyte-macrophage colony-stimulating factor (GM-CSF) increases DC number and may promote DC-dependent Treg proliferation. Here, we demonstrate that GM-CSF treatment increases CD4 CD8 DCs, which are associated with Treg expansion. In a mouse model of chronic GVHD (cGVHD), GM-CSF therapy expanded Tregs, protected against the development of skin GVHD, and regulated both Th1 and Th17 responses in the peripheral lymph nodes, resulting in an attenuation of skin cGVHD. Notably, the expanded Tregs were instrumental to GM-CSF-mediated cGVHD inhibition, which was dependent upon an increased ratio of Tregs to conventional T cells rather than augmentation of suppressive function. These data suggest that GM-CSF induces Treg proliferation by expanding CD4 CD8 DCs, which in turn regulate alloimmune responses in a cGVHD mouse model. Thus, GM-CSF could be used as a therapeutic DC modulator to induce Treg expansion and to inhibit excessive alloimmune responses in immune-related diseases.

Authors : Hotta Masaaki, Yoshimura Hideaki, Satake Atsushi, Tsubokura Yukie, Ito Tomoki, Nomura Shosaku,