Review: Granulocyte Colony-Stimulating Factor--Role and Relationships in Infectious Diseases

Dale, DC; Wc, Liles; Wr, Summer; Nelson, Steve

doi:10.1093/infdis/172.4.1061

Cited by 227 publications

(162 citation statements)

References 168 publications

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“…In this study neutralization of IL-8 with antibody blocked the transepithelial movement of PMN into the alveolar space but did not affect transendothelial cell migration, suggesting that this step is mediated by another factor. IL-1 has been shown to induce G-CSF production by macrophages and endothelial cells [12]. Our results suggest that G-CSF may have been responsible for recruitment of PMN in the interstitium of animals treated with IL-1 and neutralizing IL-8 antibody.…”

Section: Discussionmentioning

confidence: 54%

G-CSF instillation into rat lungs mediates neutrophil recruitment, pulmonary edema, and hypoxia

Hierholzer

Kelly

Lyons

et al. 1998

Journal of Leukocyte Biology

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Activated neutrophils (PMN) have been implicated in the pathogenesis of adult respiratory distress syndrome (ARDS). Granulocyte colonystimulating factor (G-CSF) is essential for PMN production and activation of PMN functions. We have recently shown that levels of G-CSF mRNA in a rat model of hemorrhagic shock correlated with severity of shock, PMN infiltration, pulmonary edema, and hypoxia. To determine whether increased tissue levels of G-CSF contribute to PMN recruitment and PMN-mediated injury, we instilled G-CSF into the lungs by intratracheal injection. Animals treated with G-CSF became hypoxic, hypocapnic, and alkalotic and demonstrated increased BAL fluid cellularity compared with control animals. The wet-to-dry ratio increased significantly after G-CSF instillation and peaked at 12 h. Histological examination of the lungs from G-CSFtreated rats revealed marked edema and increased PMN within the interstitium and alveoli. These results indicate that the presence of G-CSF alone in the lung can lead to recruitment of PMN, lung injury, and impaired pulmonary function, suggesting that local production of G-CSF may contribute to the development of lung damage and possibly ARDS in the setting of resuscitated hemorrhagic shock.

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Section: Discussionmentioning

confidence: 54%

G-CSF instillation into rat lungs mediates neutrophil recruitment, pulmonary edema, and hypoxia

Hierholzer

Kelly

Lyons

et al. 1998

Journal of Leukocyte Biology

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“…Thus, activated T cells may affect hematopoietic progenitors both directly through the production of IL-3 (23-25), IL-4 (26-28), IL-5 (29-31), and GM-CSF (32,33), as well as indirectly through the secretion of hlL-17. Not only could hlL-17 have a long-term effect on hematopoiesis by inducing G-CSF production, but, through the induction of IL-6 and IL-8 release by stromal cells, it may also participate in the triggering of the acute neutrophilia (18,34) that permits a prompt nonspecific immune response against infectious agents (25,35,36). Incidentally, the indirect hematopoietic activity of hlL-17 might partially explain why removal of T cells from donor marrow leads to a significant reduction of engraftment (37,38).…”

Section: Resultsmentioning

confidence: 99%

T cell interleukin-17 induces stromal cells to produce proinflammatory and hematopoietic cytokines.

Fossiez¹,

Djossou²,

Chomarat³

et al. 1996

The Journal of Experimental Medicine

1,359

1,158

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SummaryAnalysis of the cDNA encoding murine interleukin (IL) 17 (cytotoxic T lymphocyte associated antigen 8) predicted a secreted protein sharing 57% amino acid identity with the protein predicted from ORF13, an open reading frame ofHerpesvirus saimiri. Here we report on the cloning of human , the human counterpart ofmurine IL-17. hlL-17 is a glycoprotein of 155 amino acids secreted as an homodimer by activated memory CD4 + T cells. Although devoid of direct effects on cells of hematopoietic origin, hlL-17 and the product of its viral counterpart, Olq.F13, stimulate epithelial, endothelial, and fibroblastic cells to secrete cytokines such as IL-6, IL-8, and granulocyte--colony-stimulating factor, as well as prostaglandin E2. Furthermore, when cultured in the presence of hlL-17, fibroblasts could sustain the proliferation of CD34 + hematopoietic progenitors and their preferential maturation into neutrophils. These observations suggest that hlL-17 may constitute (a) an early initiator of the T cell-dependent inflammatory reaction; and (b) an element of the cytokine network that bridges the immune system to hematopoiesis.T lymphocytes produce an array of small proteins that are involved in cell growth, inflammation, immunity, differentiation, and repair. These protein mediators referred to as cytokines are not produced constitutively by T cells, but rather are induced after receptor-mediated T cell activation (1, 2). Murine cytotoxic T lymphocyte associated antigen-8 (mCTLA8) 1, a cDNA previously cloned by lq.ouvier et al. (3) from a T cell subtraction library, displays some of the features ofa cytokine gene: in particular, a pre1Abbreviations used in this paper: hlL-17, human IL-17; HVS, Herpesvirus saimiri; ORF13, open reading frame 13; mCTLA8, murine cytotoxic T lymphocyte-associated antigen 8; PGE 2, prostaglandin E2; PI, PMA and ionomycin.Parts of this work were presented at

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“…Growing evidence points to a beneficial role of filgrastim in human patients [36]. In vitro studies have highlighted the priming effects of G-CSF on the antimicrobial activity of neutrophils [15,18,37,38].…”

Section: Discussionmentioning

confidence: 99%

Effects of recombinant granulocyte-colony stimulating factor administration duringMycobacterium aviuminfection in mice

Gonçalves

Appelberg

2001

Clinical and Experimental Immunology

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SUMMARY Granulocyte colony-stimulating factor (G-CSF) administration in vivo has been shown to improve the defence mechanisms against infection by different microbes. Here we evaluated a possible protective role of this molecule in a mouse model of mycobacterial infection. The administration of recombinant G-CSF promoted an extensive blood neutrophilia but failed to improve the course of Mycobacterium avium infection in C57Bl/6 or beige mice. G-CSF administration also failed to improve the efficacy of a triple chemotherapeutic regimen (clarithromycin + ethambutol + rifabutin). G-CSF treatment did not protect interleukin-10 gene disrupted mice infected with M. avium. Spleen cells from infected mice treated with G-CSF had a decreased priming for antigen-specific production of interferon gamma compared to control infected mice. Our data do not substantiate previous reports on the protective activity of G-CSF in antimycobacterial immunity using mouse models.

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Review: Granulocyte Colony-Stimulating Factor--Role and Relationships in Infectious Diseases

Cited by 227 publications

References 168 publications

G-CSF instillation into rat lungs mediates neutrophil recruitment, pulmonary edema, and hypoxia

G-CSF instillation into rat lungs mediates neutrophil recruitment, pulmonary edema, and hypoxia

T cell interleukin-17 induces stromal cells to produce proinflammatory and hematopoietic cytokines.

Effects of recombinant granulocyte-colony stimulating factor administration duringMycobacterium aviuminfection in mice

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