Granulocyte colony-stimulating factor in cerebrospinal fluid from patients with meningitis

Shimoda, Kazuya; Okamura, Seiichi; Omori, Fusayuki; Mizuno, Yumi; Hara, Toshiro; Aoki, Takeshi; Ueda, Kohji; Niho, Yoshiyuki

doi:10.1182/blood.v77.10.2214.2214

Cited by 44 publications

(13 citation statements)

References 14 publications

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“…Unlike other cytokines such as TNF-␣ or IL-1 in another experiment [23], G-CSF injected i.c. did not cause migration of leucocytes into the subarachnoid space, although the concentrations which were presumably present in the CSF in this study (Ϸ 5 g/ml and 1 g/ml) assuming a CSF volume of 2 ml, were substantially higher than those observed in humans with bacterial meningitis (mean Ϸ 1500 pg/ml [6]). For this reason, G-CSF in CSF appears not to be directly involved in granulocyte recruitment or at least will not be the only substance being responsible for the recruitment of granulocytes.…”

Section: Discussioncontrasting

confidence: 65%

“…G-CSF, and after migration into the central nervous system, release larger amounts of TNF and IL-1␤ into the CSF than leucocytes not activated by G-CSF. In humans, in the CSF increased levels of G-CSF were observed both in bacterial [6,21] and viral [22] central nervous system infections. Unlike other cytokines such as TNF-␣ or IL-1 in another experiment [23], G-CSF injected i.c.…”

Section: Discussionmentioning

confidence: 99%

“…It facilitates leucocyte adhesion [3] and diapedesis [4]. In humans, G-CSF is elevated in blood during systemic bacterial infections [5], and in the cerebrospinal fluid (CSF) during bacterial meningitis [6].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Intravenous Granulocyte Colony‐Stimulating Factor Increases the Release of Tumour Necrosis Factor and Interleukin‐1β into the Cerebrospinal Fluid, But Does Not Inhibit the Growth of Streptococcus pneumoniae in Experimental Meningitis

et al. 1999

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Granulocyte colony‐stimulating factor (G‐CSF) possesses an antimicrobial effect in several animal models of infection. To evaluate a possible effect of G‐CSF on the course of pneumococcal meningitis, rabbits infected intracisternally (i.c.) with Streptococcus pneumoniae type 3 (n = 7) received 50 μg/kg of rhG‐CSF intravenously (i.v.) 1 h prior to infection. Seven infected animals served as controls. Uninfected rabbits received 10 μg of G‐CSF (n = 3), 2 μg G‐CSF (n = 3) or saline (n = 3) i.c. G‐CSF injected i.c. did not produce cerebrospinal fluid (CSF) leucocytosis. Compared with the control group, i.v. G‐CSF given prior to i.c. infection increased the percentage of granulocytes in blood 6 h and 12 h after infection. Twelve hours after infection, CSF tumour necrosis factor (TNF) activity and CSF interleukin (IL)‐1β concentrations were significantly higher in G‐CSF‐treated animals. G‐CSF did not decrease bacterial growth in the subarachnoid space and the CSF leucocyte densities were not influenced. At 24 h after infection, G‐CSF did not reduce the CSF concentrations of neurone‐specific enolase and the density of apoptotic neurones in the dentate gyrus of the hippocampus. In conclusion, i.v. G‐CSF increased the concentration of pro‐inflammatory cytokines in the CSF but did not decrease the growth of Streptococcus pneumoniae in the subarachnoid space.

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Section: Discussioncontrasting

confidence: 65%

Section: Discussionmentioning

confidence: 99%

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Intravenous Granulocyte Colony‐Stimulating Factor Increases the Release of Tumour Necrosis Factor and Interleukin‐1β into the Cerebrospinal Fluid, But Does Not Inhibit the Growth of Streptococcus pneumoniae in Experimental Meningitis

et al. 1999

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“…In contrast to stimulation with GM-CSF or M-CSF, microglial cells do not proliferate in response to G-CSF . G-CSF is also detected in the CSF of patients with meningitis (Shimoda et al, 1991).…”

Section: Central Nervous Systemmentioning

confidence: 99%

Cytokines and tumors of the central nervous system

Meir¹

1995

Glia

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Cytokines are a group of molecules with an extremely broad range of activities on a variety of target cells. This review summarizes the known cytokine and cytokine receptor expression in primary brain tumors and derived cell lines. These expression patterns are compared with those occurring in other CNS diseases, such as virus or bacterial infections, experimental allergic encephalitis, multiple sclerosis, and trauma. A variety of cytokines are expressed during CNS neoplasia; their potential involvement in tumor growth through a variety of mechanisms, such as autocrine or paracrine growth stimulation, angiogenesis, and immune surveillance evasion, are discussed. Finally, results of preliminary therapeutic approaches with cytokines are critically evaluated.

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“…A variety of cytokines play critical roles in local inflammatory responses in bacterial and aseptic meningitis [3][4][5][6]. We [7][8][9][10] and other investigators [3][4][5][6]11] showed that levels of the following cytokines increase in the cerebrospinal fluid (CSF) of aseptic meningitis: IL-1, IL-6, IL-10, interferon-gamma (IFN-g), macrophage inflammatory protein-1a (MIP-1a) and colony-stimulating factors, but not TNF-a. Aseptic meningitis is characterized by an initial accumulation in the CSF of neutrophils followed by an elevation of mononuclear cells [8,9].…”

Section: Introductionmentioning

confidence: 96%

The production of IL-8 in cerebrospinal fluid in aseptic meningitis of children

Ishiguro

Suzuki

Inaba

et al. 1997

Clinical and Experimental Immunology

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SUMMARYNeutrophils accumulate initially in the cerebrospinal fluid (CSF) of aseptic meningitis, perhaps because of increased levels of granulocyte colony-stimulating factor (G-CSF), macrophage inflammatory protein-1a (MIP-1a), and IL-8 in the subarachnoid space. We studied levels of these cytokines in children with aseptic meningitis using ELISA. When meningeal symptoms existed, IL-8 levels (1399 Ϯ 1600 ng/l, n ¼ 32) in the CSF were significantly higher than those either after meningeal symptoms disappeared (61 Ϯ 56 ng/l, n ¼ 18) or in controls (44 Ϯ 63 ng/l, n ¼ 27) ( P < 0 . 0001). High levels of IL-8 on admission dropped sequentially. Significant correlations were found between IL-8 levels and either neutrophil counts (r ¼ 0 . 612), G-CSF levels (r ¼ 0 . 873) or MIP-1a levels (r ¼ 0 . 623) in the CSF of the affected patients (P < 0 . 0001). IL-8 values in serum were lower than in the corresponding CSF samples from all individuals with meningeal symptoms. The IL-8 mRNA was detectable by reverse-transcribed polymerase chain reaction (PCR)-assisted amplification in fresh leucocytes from the CSF, but not from the peripheral blood of a healthy volunteer. The culture of CSF mononuclear cells produced high levels of IL-8 (ϳ 2750 ng/l). These data indicate that IL-8 levels rise transiently at the initial stage of aseptic meningitis, and that mononuclear cells that migrate into the CSF are a cellular source of this chemokine. We suppose that IL-8, in addition to G-CSF and MIP-1a, contribute to the localized neutrophil accumulation during the disease.

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Granulocyte colony-stimulating factor in cerebrospinal fluid from patients with meningitis

Cited by 44 publications

References 14 publications

Intravenous Granulocyte Colony‐Stimulating Factor Increases the Release of Tumour Necrosis Factor and Interleukin‐1β into the Cerebrospinal Fluid, But Does Not Inhibit the Growth of Streptococcus pneumoniae in Experimental Meningitis

Intravenous Granulocyte Colony‐Stimulating Factor Increases the Release of Tumour Necrosis Factor and Interleukin‐1β into the Cerebrospinal Fluid, But Does Not Inhibit the Growth of Streptococcus pneumoniae in Experimental Meningitis

Cytokines and tumors of the central nervous system

The production of IL-8 in cerebrospinal fluid in aseptic meningitis of children

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