Transient elevation of granulocyte colony-stimulating factor levels in cerebrospinal fluid at the initial stage of aseptic meningitis in children

• Published in: Pediatric research Vol. 37; no. 2; pp. 160 - 164
• Main Authors: FUKUSHIMA, K, ISHIGURO, A, SHIMBO, T
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 01.02.1995
• Subjects: Adolescent; Animals; Antibodies, Viral - classification; Biological and medical sciences; Cells, Cultured; Cercopithecus aethiops; Cerebrospinal Fluid Proteins - analysis; Cerebrospinal fluid. Meninges. Spinal cord; Child; Child, Preschool; Echovirus Infections - cerebrospinal fluid; Enterovirus B, Human - immunology; Enterovirus B, Human - isolation & purification; Female; Granulocyte Colony-Stimulating Factor - blood; Granulocyte Colony-Stimulating Factor - cerebrospinal fluid; HeLa Cells; Humans; Infant; Macaca fascicularis; Male; Medical sciences; Meningitis, Aseptic - blood; Meningitis, Aseptic - cerebrospinal fluid; Meningitis, Aseptic - virology; Nervous system (semeiology, syndromes); Neurology; Neutrophils - physiology; Vero Cells; Virus Cultivation; Human; Nervous system diseases; Immune response; Cytokine; Granulocyte; Exploration; Infant; Early stage; Cerebrospinal fluid; Granulocyte colony stimulating factor; Polypeptide; Central nervous system disease; Adolescent; Meningitis; Neutrophil; Child
• ISSN: 0031-3998; 1530-0447
• DOI: 10.1203/00006450-199502000-00006

At the early stage of aseptic meningitis, there is a transient increase in neutrophil counts in the cerebrospinal fluid. Some factors in the cerebrospinal fluid might induce migration of neutrophils into the cerebrospinal fluid. Granulocyte colony-stimulating factor (G-CSF) plays an important role, not only as a hemopoietic factor but also as a regulating factor for a biologic defense system by neutrophils in the foci of infection. To analyze the role of G-CSF on accumulating neutrophils in the cerebrospinal fluid, we have measured G-CSF levels in the cerebrospinal fluid of children with aseptic meningitis, paying particular attention to the phasal transition. Within the first 2 d from the onset, G-CSF levels in the cerebrospinal fluid were 223 +/- 97 ng/L, significantly higher than those of the patients without meningitis (p < 0.01). Beyond the second day after the onset, the G-CSF levels rapidly decreased to below the detectable level, even though the patients manifested meningeal signs and symptoms. There was a direct relationship between G-CSF levels and neutrophil counts in the cerebrospinal fluid (r = 0.763, p < 0.01). During the first 2 d after the onset, the G-CSF level in the cerebrospinal fluid in each case was remarkably higher than that in the serum. This finding suggests that the G-CSF in the cerebrospinal fluid was produced in the spinal cavity. From our results, the transient elevation of G-CSF levels might lead to the transient increase in neutrophil counts in the cerebrospinal fluid by recruiting them from the peripheral blood at the initial stage of aseptic meningitis.