The effect of GM-CSF and G-CSF on human neutrophil function
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Effects of polysaccharide intercellular adhesin (PIA) in an ex vivo model of whole blood killing and in prosthetic joint infection (PJI): A role for C5a
2015, International Journal of Medical MicrobiologyCitation Excerpt :This has previously been shown to control neutrophil activation and is a strong candidate for the mechanism of suppression in this model (Hartl et al., 2007). Others have suggested that dexamethasone causes suppression of neutrophil phagocytosis (Bober et al., 1995) and free radical release (Liu et al., 2014). These results are consistent with the increased risk of biofilm infections in immunocompromised patients (Weisser et al., 2010) and the immunosuppressive conditions produced during the foreign body response following the implantation of a medical device (Higgins et al., 2009; Wagner et al., 2003, 2004).
G-CSF: From granulopoietic stimulant to bone marrow stem cell mobilizing agent
2014, Cytokine and Growth Factor ReviewsCitation Excerpt :G-CSF can inhibit neutrophil apoptosis [16], increasing survival within infected tissues [17]. Although G-CSF does not directly induce the chemotaxis of neutrophils it has chemokinetic activity on these cells, promoting non-directional motility [18], which increases responses to chemotactic factors such as the bacterial agent N-Formyl-Methionine-Leucine-Phenylalanine (fMLP) [19]. Whether this contributes to the increased accumulation of neutrophils in inflamed tissues is not certain but G-CSF does not promote neutrophil migration through TNF-α activated endothelium [18].
Granulocyte-Colony Stimulating Factor (G-CSF) induces mechanical hyperalgesia via spinal activation of MAP kinases and PI<inf>3</inf>K in mice
2011, Pharmacology Biochemistry and BehaviorCitation Excerpt :For instance, granulocyte-CSF (G-CSF) enhances the production of neutrophils by inducing the proliferation and differentiation of its myeloid progenitor (Welte et al., 1985; Demetri and Griffin, 1991). G-CSF also activates terminally differentiated neutrophils by enhancing antibody-dependent killing, phagocytic activity and priming the respiratory burst (Bober et al., 1995). In agreement, G-CSF and G-CSF receptor deficient mice are severely neutropenic and susceptible to infections (Lieschke et al., 1994; Liu et al., 1996; Zhan et al., 1998; Battiwalla and McCarthy, 2009).
Cancer therapeutic antibodies come of age: Targeting minimal residual disease
2007, Molecular OncologyCitation Excerpt :Some observations suggest that the outcome of patients who receive Rituximab can be improved if the amount and function of their immune effector cell population (in particular, NK cells) are preserved or enhanced. Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a cytokine that strongly increases the number and activity of polymorphonuclears and macrophages against opsonized targets (Bober et al., 1995). Therefore, attempts to improve Rituximab efficacy are directed toward combined treatments with GM-CSF, based upon the evidence that this cytokine can up-regulate CD20 expression on lymphoid B cells and enhance ADCC (Olivieri et al., 2005).
A new schedule of CHOP/Rituximab plus granulocyte-macrophage colony-stimulating factor is an effective rescue for patients with aggressive lymphoma failing autologous stem cell transplantation
2005, Biology of Blood and Marrow Transplantation