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

Abstract

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.

Secretion of the chemokine interleukin-8 during Japanese encephalitis virus infection

“…This production could be inhibited by pre-treatment of microglia by antiin¯ammatory cytokines, i.e., IL-4, IL-10 or TGF-â. Ishiguro and his co-workers [7] have also shown the production of IL-8 in CSF during meningitis in children. IL-8 induces chemotaxis of neutrophils, releases intracellular enzymes from neutrophils and up-regulates cell adhesion molecules, potentially aiding leucocyte traf®cking across the blood±brain barrier (BBB) [23].…”

“…The present study showed very high concentrations of IL-8 in CSF during the acute stage of the illness in the majority of the patients with JE, which corresponded with the degree of severity of the disease. Although a transient increase in the level of IL-8 in CSF has been observed in patients with viral aseptic meningitis [18], bacterial pyogenic meningitis [7] or self-resolving aseptic meningitis [19], its role in viral encephalitis is not clear.…”

“…The in¯ammation results in an increased level of these cytokines in the cerebrospinal¯uid (CSF) [7]. Chemokines fall into four categories which are de®ned by a cysteine motif: CXC, CC, C and CX 3 C ± where C is cysteine and X is any amino-acid residue [8].…”

Chemotactic Factors in Cerebrospinal Fluid during Bacterial Meningitis

“…In CSF from controls (without inflammatory CNS diseases), little if any CXCL8 is detectable. However, during both bacterial (23, 40-42, 50, 67, 68, 72, 86) and aseptic (27,34,40,50,72) meningitis, a significant upregulation of CXCL8 has been demonstrated. Some (23) but not all (72) studies reported increased serum CXCL8 levels in patients with bacterial meningitis.…”

Upregulation of RANTES Gene Expression in Neuroglia by Japanese Encephalitis Virus Infection

“…Despite the pathological and socioeconomic importance of JEV, knowledge of the immunological mechanisms occurring during viral infection is limited. The inflammatory response observed within the CNS in viral encephalitis is partly mediated by chemokines, which are released by various cells of the CNS (32). Previously, we had reported that infection of astrocytes with JEV stimulated RANTES expression (16).…”