Divergent cerebrospinal fluid cytokine network induced by non-viral and different viral infections on the central nervous system

• Published in: BMC infectious diseases 2015-08, Vol.15 (1), p.345-345, Article 345
• Main Authors: Bastos, Michele Souza, Coelho-Dos-Reis, Jordana Grazziela, Zauli, Danielle Alves Gomes, Naveca, Felipe Gomes, Monte, Rossicleia Lins, Pimentel, João Paulo, Macário, Valéria Munique Kramer, da Silva, Natália Lessa, Peruhype-Magalhães, Vanessa, Pascoal-Xavier, Marcelo Antônio, Guimaraes, Allyson, Carvalho, Andréa Teixeira, Malheiro, Adriana, Martins-Filho, Olindo Assis, Mourão, Maria Paula Gomes
• Format: Article
• Language: English
• Subjects: Arbovirus Infections - cerebrospinal fluid; Arbovirus Infections - diagnosis; Arbovirus Infections - immunology; Cancer; Care and treatment; Central Nervous System Viral Diseases - cerebrospinal fluid; Central Nervous System Viral Diseases - diagnosis; Central Nervous System Viral Diseases - immunology; Chemotherapy; Coinfection - cerebrospinal fluid; Coinfection - immunology; Complications and side effects; Cross-Sectional Studies; Cytokines - cerebrospinal fluid; Cytokines - immunology; Development and progression; DNA, Viral - cerebrospinal fluid; Enterovirus Infections - cerebrospinal fluid; Enterovirus Infections - diagnosis; Enterovirus Infections - immunology; Health aspects; Herpesviridae Infections - cerebrospinal fluid; Herpesviridae Infections - diagnosis; Herpesviridae Infections - immunology; HIV (Viruses); HIV Infections - cerebrospinal fluid; HIV Infections - diagnosis; HIV Infections - immunology; Humans; Inflammation; Interferon-gamma - cerebrospinal fluid; Interferon-gamma - immunology; Interleukin-10 - cerebrospinal fluid; Interleukin-10 - immunology; Interleukin-12 - cerebrospinal fluid; Interleukin-12 - immunology; Interleukin-17 - cerebrospinal fluid; Interleukin-17 - immunology; Interleukin-6 - cerebrospinal fluid; Interleukin-6 - immunology; Lentivirus Infections - cerebrospinal fluid; Lentivirus Infections - immunology; Medical equipment and supplies industry; Medical test kit industry; Meningoencephalitis - cerebrospinal fluid; Meningoencephalitis - diagnosis; Meningoencephalitis - immunology; Patient outcomes; RNA, Viral - cerebrospinal fluid; Tumor Necrosis Factor-alpha - cerebrospinal fluid; Tumor Necrosis Factor-alpha - immunology
• ISSN: 1471-2334; 1471-2334
• DOI: 10.1186/s12879-015-1035-4

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. 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. 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). 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.