Interleukin-8 in Serum and Cerebrospinal Fluid from Patients with Meningococcal Disease

Halstensen, Alfred; Ceska, M.; Brandtzæg, Petter; Redl, Heinz; Naess, A; Waage, Anders

doi:10.1093/infdis/167.2.471

Cited by 104 publications

(71 citation statements)

References 7 publications

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“…The finding of elevated pro-and anti-inflammatory cytokines in meningococcal disease demonstrated in this study confirm those previously published [1,2,13]. Unfortunately, due to limited plasma volumes available, we were unable to measure IL-10, which has previously been shown to be an important mediator.…”

Section: Discussionsupporting

confidence: 83%

A predominantly anti-inflammatory cytokine profile is associated with disease severity in meningococcal sepsis

et al. 2005

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Objective-This study aimed to determine whether an anti-inflammatory profile in meningococcal disease is associated with an increased risk of severe disease or septic shock.Design and setting-Prospective observational study in a tertiary care children's hospital. Patients and participants-63 children with confirmed meningococcal disease.Interventions-Plasma concentrations of interleukin-1 receptor antagonist (IL-1Ra), interleukin-6 (IL-6), interleukin-8 (IL-8) and tumour necrosis factor-α (TNF) were assayed on admission. Receiver operator characteristic curve analysis was used to determine optimum thresholds for IL-1Ra:TNF, IL-1Ra:IL-6 and IL-1Ra:IL-8 ratios.Measurements and results-Median IL-1Ra:TNF and IL-1Ra:IL-6 ratios were significantly higher in severe disease with septic shock than in severe disease without septic shock and in non severe disease (IL-1Ra:TNF 263 vs. 185 vs. 108; IL-1Ra:IL-6 139 vs. 23 vs. 17). Median IL-1Ra:IL-8 ratios were not significantly different in the three groups. A significantly larger proportion of children with high IL-1Ra:TNF-α and IL-1Ra:IL-6 ratios developed severe disease with septic shock than those with a low ratios (95.2% vs. 4.8%; 76.2% vs. 23 .8%).Conclusions-An anti-inflammatory profile appears to be associated with the development of severe disease and septic shock in meningococcal sepsis. This may imply that experimental new therapies of pro-inflammatory cytokine inhibition and anti-inflammatory cytokines in meningococcal disease could be detrimental.

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Section: Discussionsupporting

confidence: 83%

A predominantly anti-inflammatory cytokine profile is associated with disease severity in meningococcal sepsis

et al. 2005

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“…It is probable that veins in the SAS, and not the choroid plexi (45), are the primary routes of entry for bacteria into the CSF, since meningococci are unable to penetrate the tight junctions of the choroidal epithelium (36) and ventriculitis is only a late complication of bacterial infection. Due to the absence of opsonophagocytic host defense in the CSF (58), uncontrolled proliferation of meningococci is followed by an inflammatory response, centered on the leptomeninges and the SAS, which is characterized by the liberation of proinflammatory cytokines and chemoattractant cytokines (chemokines) (16,55,54).…”

mentioning

confidence: 99%

Interaction ofNeisseria meningitidiswith Human Meningeal Cells Induces the Secretion of a Distinct Group of Chemotactic, Proinflammatory, and Growth-Factor Cytokines

et al. 2002

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The interactions of Neisseria meningitidis with cells of the leptomeninges are pivotal events in the progression of bacterial leptomeningitis. An in vitro model based on the culture of human meningioma cells was used to investigate the role of the leptomeninges in the inflammatory response. Following challenge with meningococci, meningioma cells secreted specifically the proinflammatory cytokine interleukin-6 (IL-6), the CXC chemokine IL-8, the CC chemokines monocyte chemoattractant protein 1 (MCP-1) and regulated-upon-activation, normal-T-cell expressed and secreted protein (RANTES), and the cytokine growth factor granulocyte-macrophage colony-stimulating factor (GM-CSF). A temporal pattern of cytokine production was observed, with early secretion of IL-6, IL-8, and MCP-1 followed by later increases in RANTES and GM-CSF levels. IL-6 was induced equally by the interactions of piliated and nonpiliated meningococci, whereas lipopolysaccharide (LPS) had a minimal effect, suggesting that other, possibly secreted, bacterial components were responsible. Induction of IL-8 and MCP-1 also did not require adherence of bacteria to meningeal cells, but LPS was implicated. In contrast, efficient stimulation of RANTES by intact meningococci required pilus-mediated adherence, which served to deliver increased local concentrations of LPS onto the surface of meningeal cells. Secretion of GM-CSF was induced by pilus-mediated interactions but did not involve LPS. In addition, capsule expression had a specific inhibitory effect on GM-CSF secretion, which was not observed with IL-6, IL-8, MCP-1, or RANTES. Thus, the data demonstrate that cells of the leptomeninges are not inert but are active participants in the innate host response during leptomeningitis and that there is a complex relationship between expression of meningococcal components and cytokine induction.Meningitis, which is an inflammation of the meninges that surround the brain within the skull and the spinal cord within the spinal canal (56), is the most common infection of the central nervous system. In humans, the meninges comprise the pachymenix or dura mater (hard mother) and the leptomeninges, which consist of the arachnoid mater and pia mater together with the trabeculae that traverse the cerebrospinal fluid (CSF)-filled subarachnoid space (SAS) (2, 9, 56). Classical bacterial meningitis is predominantly a leptomeningitis, with little or no involvement of the dura mater or the underlying brain. The bacterial etiology of leptomeningitis is broad, and a wide variety of bacteria that gain access to the SAS can initiate an inflammatory response. Susceptibility to the various causative agents is age dependent, and a distinct group of species affect neonates compared to the species that affect subjects over 1 month old (13). After the neonatal period, the most common bacterial agents that cause pyogenic leptomeningitis are Haemophilus influenzae, Streptococcus pneumoniae, and Neisseria meningitidis (meningococci). In affluent countries, vaccines developed against H. inf...

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“…Lipopolysaccharide (LPS) released from Gram-negative bacteria such as meningococci initiate the production of pro-inflammatory cytokines by cells of the mononuclear-macrophage lineage and endothelial cells. Circulating levels of these cytokines, including tumor necrosis factor (TNF)-a, interleukin (IL)-1, 1 IL-6, 1,2 IL-8, 3 and IL-10, 4,5 are increased in children with septic shock and purpura. Severity of disease is related to the initial plasma levels of LPS 6 and of these cytokines.…”

mentioning

confidence: 99%

Interleukin 12 Levels During the Initial Phase of Septic Shock With Purpura in Children: Relation to Severity of Disease

et al. 1997

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Interleukin-8 in Serum and Cerebrospinal Fluid from Patients with Meningococcal Disease

Cited by 104 publications

References 7 publications

A predominantly anti-inflammatory cytokine profile is associated with disease severity in meningococcal sepsis

A predominantly anti-inflammatory cytokine profile is associated with disease severity in meningococcal sepsis

Interaction ofNeisseria meningitidiswith Human Meningeal Cells Induces the Secretion of a Distinct Group of Chemotactic, Proinflammatory, and Growth-Factor Cytokines

Interleukin 12 Levels During the Initial Phase of Septic Shock With Purpura in Children: Relation to Severity of Disease

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