RESUMEN
BACKGROUND: Meningoencephalitis is one of the most common disorders of the central nervous system (CNS) worldwide. Viral meningoencephalitis differs from bacterial meningitis in several aspects. In some developing countries, bacterial meningitis has appropriate clinical management and chemotherapy is available. Virus-associated and virus not detected meningoencephalitis are treatable, however, they may cause death in a few cases. The knowledge of how mediators of inflammation can induce disease would contribute for the design of affordable therapeutic strategies, as well as to the diagnosis of virus not detected and viral meningoencephalitis. Cytokine-induced inflammation to CNS requires several factors that are not fully understood yet. METHODS: Considering this, several cytokines were measured in the cerebrospinal fluid (CSF) of patients with undiagnosed and viral meningoencephalitis, and these were correlated with cellularity in the CSF. RESULTS: The results demonstrate that an altered biochemical profile alongside increased cellularity in the cerebrospinal fluid is a feature of patients with meningoencephalitis that are not associated with the detection of virus in the CNS (P < 0.05). Moreover, HIV-positive patients (n = 10) that evolve with meningoencephalitis display a distinct biochemical/cytological profile (P < 0.05) in the cerebrospinal fluid. Meningoencephalitis brings about a prominent intrathecal cytokine storm regardless of the detection of virus as presumable etiological agent. In the case of Enterovirus infection (n = 13), meningoencephalitis elicits robust intrathecal pro-inflammatory cytokine pattern and elevated cellularity when compared to herpesvirus (n = 15) and Arbovirus (n = 5) viral infections (P < 0.05). CONCLUSION: Differences in the cytokine profile of the CSF may be unique if distinct, viral or presumably non-viral pathways initially trigger the inflammatory response in the CNS.
Asunto(s)
Infecciones por Arbovirus/líquido cefalorraquídeo , Citocinas/líquido cefalorraquídeo , Infecciones por Enterovirus/líquido cefalorraquídeo , Infecciones por VIH/líquido cefalorraquídeo , Infecciones por Herpesviridae/líquido cefalorraquídeo , Infecciones por Lentivirus/líquido cefalorraquídeo , Meningoencefalitis/líquido cefalorraquídeo , Infecciones por Arbovirus/diagnóstico , Infecciones por Arbovirus/inmunología , Enfermedades Virales del Sistema Nervioso Central/líquido cefalorraquídeo , Enfermedades Virales del Sistema Nervioso Central/diagnóstico , Enfermedades Virales del Sistema Nervioso Central/inmunología , Coinfección/líquido cefalorraquídeo , Coinfección/inmunología , Estudios Transversales , Citocinas/inmunología , ADN Viral/líquido cefalorraquídeo , Infecciones por Enterovirus/diagnóstico , Infecciones por Enterovirus/inmunología , Infecciones por VIH/diagnóstico , Infecciones por VIH/inmunología , Infecciones por Herpesviridae/diagnóstico , Infecciones por Herpesviridae/inmunología , Humanos , Inflamación , Interferón gamma/líquido cefalorraquídeo , Interferón gamma/inmunología , Interleucina-10/líquido cefalorraquídeo , Interleucina-10/inmunología , Interleucina-12/líquido cefalorraquídeo , Interleucina-12/inmunología , Interleucina-17/líquido cefalorraquídeo , Interleucina-17/inmunología , Interleucina-6/líquido cefalorraquídeo , Interleucina-6/inmunología , Infecciones por Lentivirus/inmunología , Meningoencefalitis/diagnóstico , Meningoencefalitis/inmunología , ARN Viral/líquido cefalorraquídeo , Factor de Necrosis Tumoral alfa/líquido cefalorraquídeo , Factor de Necrosis Tumoral alfa/inmunologíaRESUMEN
Aging continuously remodels the immune system, a process known as immunosenescence. Here, we review evidence of premature immunosenescence in younger individuals under conditions of chronic psychological stress, chronic inflammation, or exposure to certain persistent viral infections. Chronic stress may accelerate various features of immunosenescence by activating key allostatic systems, notably the hypothalamic-pituitary-adrenal axis and increased cortisol levels. Chronic stress is associated with thymic involution, blunted T cell proliferation, increased serum proinflammatory markers, and shorter telomere lengths. Human cytomegalovirus (CMV) infection has been implicated in accelerating immunosenescence by shrinking the T cell receptor repertoire and causing clonal expansion of senescent CD8(+) CD28(-) T cells with a proinflammatory profile. These factors increase inflammation associated with aging, or "inflammaging," particularly as it relates to etiology of several age-related diseases and increased mortality. Patients with rheumatoid arthritis have been shown to have several signatures of premature immunosenescence, including expansion of senescent T cells associated with cognitive impairment. We end by speculating that bipolar disorder can be considered as a model of accelerated aging because it has been associated with shortened telomeres, higher CMV IgG titers, and expansion of senescent and regulatory T cells.