Recombinant Human Macrophage Colony-Stimulating Factor Augments Pulmonary Host Defences Against Aspergillus Fumigatus

Gonzalez, Corina E.; Lyman, Caron A.; Lee, Sondra; Guercio, Carla Del; Roilides, Emmanuel; Bacher, John; Gehrt, Andreas; Feuerstein, Erwin; Tsokos, Maria; Walsh, Thomas J.

doi:10.1006/cyto.2001.0889

Cited by 33 publications

(16 citation statements)

References 44 publications

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“…M-CSF augments the activity of monocytes/macrophages against P. marneffei in vitro and against C. albicans and S. aureus ex vivo [46,47]. M-CSF prolonged survival when given either prophylactically in a neutropenic rabbit model of pulmonary aspergillosis or with treatment intent in an immunosuppressed mouse model of candidemia [48,49].…”

Section: Macrophage Colony-stimulating Factormentioning

confidence: 99%

Granulocyte colony-stimulating factor, granulocyte–macrophage colony-stimulating factor, and other immunomodulatory therapies for the treatment of infectious diseases in solid organ transplant recipients

Page

Liles

2008

Current Opinion in Organ Transplantation

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Section: Macrophage Colony-stimulating Factormentioning

confidence: 99%

Granulocyte colony-stimulating factor, granulocyte–macrophage colony-stimulating factor, and other immunomodulatory therapies for the treatment of infectious diseases in solid organ transplant recipients

Page

Liles

2008

Current Opinion in Organ Transplantation

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“…14 In particular, a number of in vitro and in vivo studies have shown that M-CSF activates antimicrobial activities of macrophages. [42][43][44][45] Moreover, the clinical efficacy of M-CSF has been proven in patients with invasive fungal infections. 46 …”

Section: Mechanism By Which Nef Inhibits M-csf Receptor Signalingmentioning

confidence: 99%

HIV-1 Nef interferes with M-CSF receptor signaling through Hck activation and inhibits M-CSF bioactivities

Suzu

Harada

Μatsumoto

et al. 2005

Blood

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IntroductionNef is an accessory protein of HIV-1, a causative virus for AIDS. A number of reports, including studies of HIV-1-infected patients and of animal models, have demonstrated that the Nef protein is a major determinant of the pathogenicity of HIV-1. [1][2][3][4] Transgenic mice expressing the complete coding sequences of HIV-1 under the regulatory sequences of human CD4 gene developed severe AIDS-like abnormalities: loss of CD4 ϩ T cells, thymus atrophy, failure to thrive, diarrhea, wasting, premature death, interstitial pneumonitis, and tubulo-interstitial nephritis. 4 Using this mouse model and the introduction of mutation into selected HIV-1 gene(s), Hanna et al 4 clearly demonstrated that Nef harbored a major disease determinant. Therefore, much attention has been given to Nef to explain its contribution to HIV-1 pathogenesis and to investigate it as a target for antiviral drug development.CD4 ϩ T cells and monocytes/macrophages are the principal target cells for HIV-1, and the functions of Nef in CD4 ϩ T cells are generally accepted as accounting for many aspects of viral pathogenesis (reviewed in Fackler and Baur 5 and Peterlin and Trono 6 ). For example, Nef has been shown to cause the downregulation of cell surface molecules such as cell surface receptor CD4 7 and major histocompatibility complex (MHC) class I in CD4 ϩ T cells. 8 The down-regulation of MHC class I is considered to diminish the recognition of HIV-1-infected cells by cytotoxic T cells. In contrast, the contribution of monocytes/macrophages to viral pathogenesis is less well understood. Several lines of evidence support the idea that monocytes/macrophages and CD4 ϩ T cells are important for the development and progression of AIDS. Recent studies have demonstrated that Nef induces the production of CC chemokines (macrophage inflammatory proteins-1␣ and -1␤) and soluble forms of CD23 and intracellular adhesion molecule-1 by macrophages. 9,10 These Nef-induced factors from macrophages might stimulate the chemotaxis and activation of resting CD4 ϩ T cells, thereby promoting the permissiveness of CD4 ϩ T cells to HIV-1 infection. 9,10 This Nef function is likely to be mediated by the activation of NF-B transcription factor. 10 Another important feature of Nef is the binding at high affinity to myeloid lineage-specific Src family kinase Hck to activate its kinase activity. 11,12 The proline-rich (PxxP) motif in Nef binds to the Src homology 3 (SH3) domain of Hck. 11 Interestingly, Hck was found to bind preferentially and with higher affinity to Nef than other Src kinases. 11 The pathologic relevance of the molecular interaction in vivo was revealed by studies of HIV-1 transgenic mice. The mutation in the SH3-binding motif of Nef abolished the development of AIDS-like disease in the HIV-1 transgenic mice. 13 Moreover, the breeding of transgenic mice expressing the complete coding sequences of HIV-1 on a hck Ϫ/Ϫ background resulted in the delay of disease development. 13 These studies suggest that the modulation of macrophage functions by ...

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“…A neutropenic rabbit model demonstrated that prophylactic administration 3 days before inoculation and then throughout neutropenia augmented pulmonary host defenses against IA. Rabbits receiving M-CSF had increased survival rates and greater numbers of activated pulmonary alveolar macrophages than did control animals [358]. A phase I trial of M-CSF suggested some benefit in patients with Aspergillus infections, but an insufficient number of patients were treated to show a statistical benefit [343,359].…”

Section: Immunomodulatory Therapymentioning

confidence: 99%

Review of Newer Antifungal and Immunomodulatory Strategies for Invasive Aspergillosis

2003

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The incidence of invasive aspergillosis is markedly increasing, and mortality remains dismal. Previously there were only 2 antifungals with activity against Aspergillus, but over the last few years there has been an explosion of newer agents and reformulations of older antifungals. Exploration has also begun with immunotherapy, with use of cytokines and granulocyte transfusions alone or in combination with antifungal therapy. This review will detail the available in vitro, in vivo, and clinical experience with the newer antifungal and immunomodulatory therapies in development for treatment of invasive aspergillosis.

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Recombinant Human Macrophage Colony-Stimulating Factor Augments Pulmonary Host Defences Against Aspergillus Fumigatus

Cited by 33 publications

References 44 publications

Granulocyte colony-stimulating factor, granulocyte–macrophage colony-stimulating factor, and other immunomodulatory therapies for the treatment of infectious diseases in solid organ transplant recipients

Granulocyte colony-stimulating factor, granulocyte–macrophage colony-stimulating factor, and other immunomodulatory therapies for the treatment of infectious diseases in solid organ transplant recipients

HIV-1 Nef interferes with M-CSF receptor signaling through Hck activation and inhibits M-CSF bioactivities

Review of Newer Antifungal and Immunomodulatory Strategies for Invasive Aspergillosis

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