transforming-growth-factor-beta and Meningitis--Aseptic

We investigated the levels of transforming growth factor beta 1 (TGF-beta 1) in cerebrospinal fluid (CSF) in children with meningitis, with a view to prognostic relevance. CSF TGF-beta 1 levels on admission were measured by a sandwich enzyme immunoassay in children with bacterial meningitis (n = 16), aseptic meningitis (n = 12), and control subjects without evidence of central nervous system (CNS) infection (n = 16). Patients were followed up for a mean duration of 13 months, and neurodevelopmental sequelae was determined for those with bacterial meningitis. On admission, CSF TGF-beta 1 levels were significantly higher in children with bacterial meningitis (mean, standard error, 32.92, 2.36 pg/ml) as opposed to those with aseptic meningitis (25.26, 1.72 pg/ml) (P = 0.0155), or control subjects (20.53, 1.05 pg/ml) (P < 0.0001). The CSF TGF-beta 1 levels in children with aseptic meningitis were higher than those in the control group, but without significance (P = 0.02). No apparent correlation existed between CSF TGF-beta 1 levels and CSF protein or cell counts in patients with bacterial meningitis. No significant difference in CSF TGF-beta 1 levels was found between patients with or without major sequelae following bacterial meningitis.

Topics: Acute Disease; Child; Child, Preschool; Female; Humans; Infant; Male; Meningitis, Aseptic; Meningitis, Bacterial; Prognosis; Transforming Growth Factor beta

Mycoplasma pneumoniae sometimes causes central nervous system manifestations, which may involve the host immune response, as the organism does not directly damage neural cells, or release toxins. Therefore we measured the levels of interleukin-6, interleukin-8, interleukin-18, interferon-gamma, tumor necrosis factor-alpha, and transforming growth factor-beta1 in serum and cerebrospinal fluid samples from patients who manifested central nervous system manifestations during acute M. pneumoniae infection. The subjects were nine patients with early-onset encephalitis (central nervous system disease onset within 7 days from the onset of fever), four with late-onset encephalitis (onset at 8 days or later), three with encephalitis but without fever, and three with aseptic meningitis. Intrathecal elevations of interleukin-6 and interleukin-8 in all four types of central nervous system manifestations, and of interleukin-18 in late-onset encephalitis were observed. None of the cerebrospinal fluid samples contained detectable levels of interferon-gamma, tumor necrosis factor-alpha, or transforming growth factor-beta1. In conclusion, interleukin-6, interleukin-8, and interleukin-18 might be involved in the inflammatory process leading to the central nervous system manifestations caused by M. pneumoniae.

Topics: Adolescent; Child; Child, Preschool; Cytokines; Encephalitis; Enzyme-Linked Immunosorbent Assay; Female; Humans; Interferon-gamma; Interleukin-18; Interleukin-6; Interleukin-8; Male; Meningitis, Aseptic; Mycoplasma pneumoniae; Pneumonia, Mycoplasma; Transforming Growth Factor beta; Transforming Growth Factor beta1; Tumor Necrosis Factor-alpha

Meningitis is a serious disease mostly caused by viral or bacterial infections. In complicated cases it may lead to brain damage and death. The infection and cell damage result in a cellular and immunological response. Following this, a high secretion of cytokines can be expected. Cytokines, especially tumour necrosis factor alpha (TNF-alpha) and interleukin-1 (IL-1), promote the inflammatory reactions in the subarachnoid space. Transforming growth factor beta 1 (TGF-beta 1) has antagonistic effects on TNF-alpha and IL-1-mediated processes. Therefore, it suppresses inflammatory reactions. To observe the expression of TGF-beta 1 in transcellular signalling in the inflammatory processes of meningitis, we investigated TGF-beta 1 mRNA in cells in the cerebrospinal fluid of three patients with meningitis by non-radioactive in situ hybridization. All patients fulfilled the usual clinical criteria of meningitis. In one case Neisseria menigitidis could be identified as the pathogenic agent. In the remainder, no agent could be isolated. In all cytological preparations of the cerebrospinal fluid of these patients a high level of TGF-beta 1 mRNA was detectable in the cell populations. It was possible to distinguish between the different cell types of the cerebrospinal fluid and to attach the mRNA expression to them. On the one hand, this makes it possible to investigate pathogenesis and defence mechanisms in bacterial and aseptic meningitis on a cellular level; on the other hand, it may open new perspectives in the control of disease development, prognosis, diagnosis and supporting therapy.

Topics: Adult; Cerebrospinal Fluid; Female; Humans; In Situ Hybridization; Male; Meningitis; Meningitis, Aseptic; Meningitis, Meningococcal; Microscopy, Fluorescence; RNA, Messenger; Signal Transduction; Transforming Growth Factor beta