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Local M-CSF (Macrophage Colony-Stimulating Factor) Expression Regulates Macrophage Proliferation and Apoptosis in Atherosclerosis.

OBJECTIVE: Previous studies have shown that deficiency of M-CSF (macrophage colony-stimulating factor; or CSF1 [colony stimulating factor 1]) dramatically reduces atherosclerosis in hyperlipidemic mice. We characterize the underlying mechanism and investigate the relevant sources of CSF1 in lesions. Approach and Results: We quantitatively assessed the effects of CSF1 deficiency on macrophage proliferation and apoptosis in atherosclerotic lesions. Staining of aortic lesions with markers of proliferation, Ki-67 and bromodeoxyuridine, revealed around 40% reduction in CSF1 heterozygous (Csf1+/-) a

Use of Biosimilar Granulocyte Colony-Stimulating Factor for Mobilization in Autologous and Allogeneic Hematopoietic Stem Cell Transplantation.

The biologic medication filgrastim is approved by the Food and Drug Administration (FDA) to mobilize hematopoietic progenitor cells (HPCs) for collection by leukapheresis for autologous hematopoietic stem cell transplant (HSCT). The FDA-approved biologic tbo-filgrastim is currently used off-label for this indication in both autologous and allogeneic HSCT at the Tennessee Valley Healthcare System. The purpose of this review is to compare the efficacy of filgrastim and tbo-filgrastim for this indication. The primary outcomes were the proportion of autologous patients and allogeneic donors with a

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… To harvest an adequate number of HPCs to achieve engraftment from peripheral blood, granulocyte colony-stimulating factors (G-CSFs) must be used to mobilize HPCs from the bone marrow microenvironment into the peripheral bloodstream [ 3 ]. … factor Adv Ther 2011 28 304 10 10.1007/s12325-011-0009-1 21400232 [11] Publicover A Richardson DS Davies A Hill KS Hurlock C Hutchins D Use of a biosimilar granulocyte colony-stimulating factor for peripheral blood stem cell mobilization: an analysis of mobilization and engraftment Br J Haematol 2013 …

Granulocyte Colony-Stimulating Factor Does Not Influence Clostridium Perfringens α-Toxin-Induced Myonecrosis in Mice.

Clostridium perfringens type A causes gas gangrene characterized by myonecrosis and development of an effective therapy for treating affected patients is of clinical importance. It was recently reported that the expression of granulocyte colony-stimulating factor (G-CSF) is greatly up-regulated by C. perfringens infection. However, the role of G-CSF in C. perfringens-mediated myonecrosis is still unclear. Here, we assessed the destructive changes in C. perfringens-infected skeletal muscles and tested whether inhibition of G-CSF receptor (G-CSFR) signaling or administration of recombinant G-CSF

[Resection of a Granulocyte Colony-Stimulating Factor-Producing Anaplastic Carcinoma of the Pancreas, Associated with Humoral Hypercalcemia of Malignancy].

We herein report the case of a 65-year-old man who presented with an anaplastic carcinoma of the pancreas, producing granulocyte colony-stimulating factor (G-CSF). The patient's laboratory data showed an increase in his serum CA19-9 levels 1 year after he had undergone surgery for transverse colon cancer. Computed tomography (CT) showed a mass in the pancreatic head. Following a diagnosis of primary or metastatic pancreatic cancer, we performed the pancreatoduodenectomy. The postoperative course was uneventful. However, on postoperative day 28, he suffered a disturbance of consciousness and de

Inhibition of colony-stimulating factor 1 receptor early in disease ameliorates motor deficits in SCA1 mice.

BACKGROUND: Polyglutamine (polyQ) expansion in the protein Ataxin-1 (ATXN1) causes spinocerebellar ataxia type 1 (SCA1), a fatal dominantly inherited neurodegenerative disease characterized by motor deficits, cerebellar neurodegeneration, and gliosis. Currently, there are no treatments available to delay or ameliorate SCA1. We have examined the effect of depleting microglia during the early stage of disease by using PLX, an inhibitor of colony-stimulating factor 1 receptor (CSFR1), on disease severity in a mouse model of SCA1. METHODS: Transgenic mouse model of SCA1, ATXN1[82Q] mice, and wild

Practically feasible production of sustained-release microspheres of granulocyte-macrophage colony-stimulating factor (rhGM-CSF).

Using recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF) as a model drug, the present study demonstrated a practically feasible process to produce polymeric microspheres for sustained-release delivery of protein drugs with preserved integrity. This process is featured with pre-loading proteins into polysaccharide fine particles via a self-standing aqueous-aqueous "emulsion", prior to microencapsulation into the microspheres. The protein drug, rhGM-CSF, was partitioned thermodynamically into a dextran dispersed phase of the aqueous-aqueous emulsion, followed by lyophi

Successful Granulocyte Colony-stimulating Factor Treatment of Relapsing Candida albicans Meningoencephalitis Caused by CARD9 Deficiency.

Caspase-associated recruitment domain-9 (CARD9) deficiency is an autosomal-recessive primary immunodeficiency with genetic defects in Th17 immunity marked by susceptibility to recurrent and invasive Candida infections. We present a case of relapsing Candida albicans meningoencephalitis over 1-year period despite appropriate antifungal therapy. We detected a homozygous p.Q295X mutation in CARD9 as well as a defective interleukin-17 and interferon gamma synthesis in Enzyme-Linked ImmunoSpot tests. We achieved complete clinical remission, and improvement of interleukin-17 secretion with subcutane

Granulocyte colony-stimulating factor (G-CSF) plays an important role in immune complex-mediated arthritis.

Neutrophils are an abundant cell type in many chronic inflammatory diseases such as rheumatoid arthritis (RA); however, their contribution to the pathology of RA has not been widely studied. A key cytokine involved in neutrophil development and function is granulocyte-colony stimulating factor (G-CSF). In this study we used the K/BxN serum-transfer arthritis (STA) model, mimicking the effector phase of RA, to investigate the importance of G-CSF in arthritis development and its relation to neutrophils. Here, we show for the first time in this model that G-CSF levels are increased both in the se

Combinatorial Intervention with Mesenchymal Stem Cells and Granulocyte Colony-Stimulating Factor in a Rat Model of Ulcerative Colitis.

BACKGROUND: Bone marrow mesenchymal stem cells sometimes improve symptoms of inflammatory bowel disease. AIM: To test the effects of combined granulocyte colony-stimulating factor (G-CSF) and MSC therapy in a rat model of ulcerative colitis (UC). METHODS: Seventy-two rats with TNBS-induced UC were divided into control or treatment groups: control (no disease and no treatment), no treatment (model), 5-aminosalicylate (5-ASA) enema, or MSCs (labeled with BrdU) with (MSC/GCSF) or without (MSC) G-CSF, and G-CSF alone (GCSF). On days 14 and 28 post-treatment, macroscopic and histological appearan

Short-term effect of granulocyte colony-stimulating factor in dogs with severe myxomatous mitral valve disease.

BACKGROUND: Use of granulocyte colony-stimulating factor (G-CSF) to treat damaged myocardium is a relatively new concept. Clinical beneficial and safety outcomes are still controversial. OBJECTIVE: The aim of this study was to evaluate recruitment of hematopoietic stem cells and therapeutic efficacy of G-CSF in the treatment of myxomatous mitral valve disease (MMVD) of dogs. ANIMALS AND METHODS: Thirty client-owned MMVD dogs with clinical signs of heart failure were enrolled in a prospective double-blind, randomized, placebo-controlled study to compare the short-term effect of G-CSF (n = 17)

Failure to improve a thin endometrium in the late proliferative phase with uterine infusion of granulocyte-colony stimulating factor.

PURPOSE: To determine if the treatment with uterine infusion of granulocyte colony-stimulating factor (G-CSF) can improve endometrial thickness in an infertile woman with a double uterus, who consistently showed a thin endometrium in the late proliferative phase either in controlled ovarian hyperstimulation (COH) IVF-ET cycles or with graduated estrogen/sildenafil protocols for frozen embryo transfer (ET). MATERIALS AND METHODS: A single uterine infusion of G-CSF was performed in the late proliferative phase in a woman who only attained a five-mm thickness despite a high dose vaginal and oral

Granulocyte macrophage colony-stimulating factor treatment of a patient in myasthenic crisis: effects on regulatory T cells.

INTRODUCTION: In this study we describe a patient with a prolonged myasthenic crisis refractory to conventional immunomodulatory therapy who was treated with GM-CSF (granulocyte macrophage colony-stimulating factor, sargramostim). METHODS: T-regulatory cell (Treg) suppressive function and Foxp3 expression were evaluated before and after treatment with GM-CSF. RESULTS: Treatment with GM-CSF was associated with clinical improvement, expansion in the circulating numbers of Foxp3(+) cells, increase in Foxp3 expression levels in Tregs, early improvement in Treg suppressive capacity for AChR-α-ind

Granulocyte-macrophage colony-stimulating factor-transfected bone marrow stromal cells for the treatment of ischemic stroke.

Adult, male, Sprague-Dawley rats were injected with granulocyte-macrophage colony-stimulating factor-transfected bone marrow stromal cells (GM-CSF-BMSCs) into the ischemic boundary zone at 24 hours after onset of middle cerebral artery occlusion. Results showed reduced infarct volume, decreased number of apoptotic cells, improved neurological functions, increased angiogenic factor expression, and increased vascular density in the ischemic boundary zone in rats that underwent GM-CSF-BMSCs transplantation compared with the BMSCs group. Experimental findings suggested that GM-CSF-BMSCs could serv

A role for granulocyte-macrophage colony-stimulating factor in the regulation of CD8(+) T cell responses to rabies virus.

Inflammatory cytokines have a significant role in altering the innate and adaptive arms of immune responses. Here, we analyzed the effect of GM-CSF on a RABV-vaccine vector co-expressing HIV-1 Gag. To this end, we immunized mice with RABV expressing HIV-1 Gag and GM-CSF and analyzed the primary and recall CD8(+) T cell responses. We observed a statistically significant increase in antigen presenting cells (APCs) in the spleen and draining lymph nodes in response to GM-CSF. Despite the increase in APCs, the primary and memory anti HIV-1 CD8(+) T cell response was significantly lower. This was p

Healing of laser-induced tympanic membrane perforations in rats: no contribution of granulocyte colony-stimulating factor or Gelfoam.

OBJECTIVES: To study whether granulocyte colony-stimulating factor together with Gelfoam (absorbable gelatin sponge, USP) could enhance the healing of freshly perforated tympanic membranes. The frequency and occurrence of different immunocompetent cells and collagen types was noted. METHODS: Laser perforations were made in the tympanic membrane of rats that were sacrificed at different time intervals post-myringotomy: Day 1, 3, 6, and 12. Tympanic membrane specimens were embedded and sections were stained with hematoxylin/eosin and an immunohistochemical technique was used, with antibodies ag

Role of macrophage colony-stimulating factor (M-CSF)-dependent macrophages in gastric ulcer healing in mice.

We examined the role of macrophage colony-stimulating factor (M-CSF)-dependent macrophages in the healing of gastric ulcers in mice. Male M-CSF-deficient (op/op) and M-CSF-expressing heterozygote (+/?) mice were used. Gastric ulcers were induced by thermal cauterization under ether anesthesia, and healing was observed for 14 days after ulceration. The numbers of macrophages and microvessels in the gastric mucosa were determined immunohistochemically with anti-CD68 and anti-CD31 antibodies, respectively. Expression of tumor necrosis factor (TNF)-α, cyclooxygenase (COX)-2, and vascular endotheli

Interferon-α suppressed granulocyte colony stimulating factor production is reversed by CL097, a TLR7/8 agonist.

BACKGROUND AND AIM: Neutropenia, a major side-effect of interferon-α (IFN-α) therapy can be effectively treated by the recombinant form of granulocyte colony stimulating factor (G-CSF), an important growth factor for neutrophils. We hypothesized that IFN-α might suppress G-CSF production by peripheral blood mononuclear cells (PBMCs), contributing to the development of neutropenia, and that a toll-like receptor (TLR) agonist might overcome this suppression. METHODS: Fifty-five patients who were receiving IFN-α/ribavirin combination therapy for chronic hepatitis C virus (HCV) infection were rec

Long-term evaluation of granulocyte-colony stimulating factor on hypoxic-ischemic brain damage in infant rats.

PURPOSE: Hypoxia-ischemia (HI), as a major cause of fetal brain damage, has long-lasting neurological implications. Therefore, therapeutic interventions that attenuate the neuropathological outcome of HI while also improving the neurofunctional outcome are of paramount clinical importance. The aim of this study was to investigate the long-term functional and protective actions of granulocyte-colony stimulating factor (G-CSF) treatment in an experimental model of cerebral HI. METHODS: Postnatal day-7 Sprague-Dawley rats were subjected to HI surgery, which entailed ligation of the right common

Detection of M2 macrophages and colony-stimulating factor 1 expression in serous and mucinous ovarian epithelial tumors.

Tumor-associated macrophages (TAM) are known to possess the immunosuppressive M2 macrophage phenotype. They contribute to tumor growth, invasion, and metastasis by producing various mediators. Macrophages, especially M2 polarized macrophages, preferentially express CD163 and CD204, but few studies have investigated macrophage phenotypes in human ovarian tumors. The purpose of the present study was therefore to present results on macrophage differentiation in human ovarian serous and mucinous epithelial tumors. The method focused on immunostaining of paraffin-embedded tumor samples. Almost all