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

Bastos MS, Coelho-Dos-Reis JG, Zauli DA, Naveca FG, Monte RL, Pimentel JP, Macário VM, da Silva NL, Peruhype-Magalhães V, Pascoal-Xavier MA, Guimaraes A, Carvalho AT, Malheiro A, Martins-Filho OA, Mourão MP - BMC Infect. Dis. (2015)

Bottom Line: 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).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.

View Article: PubMed Central - PubMed

Affiliation: Tropical Medicine Foundation Dr. Heitor Vieira Dourado, Manaus, AM, Brazil. michelebastos01@gmail.com.

ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus

Cerebrospinal fluid cellularity was measured in control samples, virus not detected (undiagnosed) and virus-positive patients with meningoencephalitis (a) as described in material and methods. Results are expressed as number of cells per field (#cells/field). The global median of meningoencephalitis group was calculated and employed as a cut off point to discriminate patients with low and high cellularity. Percentages of high cellularity are displayed for virus not detected (undiagnosed) and virus-positive patients with aseptic meningitis. b Virus not detected (undiagnosed) and virus-positive patients with meningoencephalitis were classified as with either high or low cellularity and subdivided in two groups. The levels of the cytokines IL-6, IL-12, IL-17, TNF-α, IFN-γ and IL-10 (expressed as Mean Fluorescence Intensity-MFI) of the subgroups were compared. Statistical differences between subgroups within the same group are highlighted as connecting lines or # and differences between groups (black versus gray) were highlighted as *. The median values for each cytokine measured in the control sample are represented by a dotted line in each graph
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Fig3: Cerebrospinal fluid cellularity was measured in control samples, virus not detected (undiagnosed) and virus-positive patients with meningoencephalitis (a) as described in material and methods. Results are expressed as number of cells per field (#cells/field). The global median of meningoencephalitis group was calculated and employed as a cut off point to discriminate patients with low and high cellularity. Percentages of high cellularity are displayed for virus not detected (undiagnosed) and virus-positive patients with aseptic meningitis. b Virus not detected (undiagnosed) and virus-positive patients with meningoencephalitis were classified as with either high or low cellularity and subdivided in two groups. The levels of the cytokines IL-6, IL-12, IL-17, TNF-α, IFN-γ and IL-10 (expressed as Mean Fluorescence Intensity-MFI) of the subgroups were compared. Statistical differences between subgroups within the same group are highlighted as connecting lines or # and differences between groups (black versus gray) were highlighted as *. The median values for each cytokine measured in the control sample are represented by a dotted line in each graph

Mentions: The cellularity in the CSF was evaluated in patients with meningoencephalitis and healthy controls (Fig. 3). All patients with meningoencephalitis had cellularity above this threshold and controls had cellularity below it. Using the total number of samples, a global median was calculated in order to establish an internal cut off point to differentiate low from high cellularity. Patients with viral meningoencephalitis displayed higher frequency of high cellularity (55 %) when compared with meningoencephalitis patients without viral infection (38 %), however this difference was not statistically significant (Fig. 3a).Fig. 3


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

Bastos MS, Coelho-Dos-Reis JG, Zauli DA, Naveca FG, Monte RL, Pimentel JP, Macário VM, da Silva NL, Peruhype-Magalhães V, Pascoal-Xavier MA, Guimaraes A, Carvalho AT, Malheiro A, Martins-Filho OA, Mourão MP - BMC Infect. Dis. (2015)

Cerebrospinal fluid cellularity was measured in control samples, virus not detected (undiagnosed) and virus-positive patients with meningoencephalitis (a) as described in material and methods. Results are expressed as number of cells per field (#cells/field). The global median of meningoencephalitis group was calculated and employed as a cut off point to discriminate patients with low and high cellularity. Percentages of high cellularity are displayed for virus not detected (undiagnosed) and virus-positive patients with aseptic meningitis. b Virus not detected (undiagnosed) and virus-positive patients with meningoencephalitis were classified as with either high or low cellularity and subdivided in two groups. The levels of the cytokines IL-6, IL-12, IL-17, TNF-α, IFN-γ and IL-10 (expressed as Mean Fluorescence Intensity-MFI) of the subgroups were compared. Statistical differences between subgroups within the same group are highlighted as connecting lines or # and differences between groups (black versus gray) were highlighted as *. The median values for each cytokine measured in the control sample are represented by a dotted line in each graph
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4541733&req=5

Fig3: Cerebrospinal fluid cellularity was measured in control samples, virus not detected (undiagnosed) and virus-positive patients with meningoencephalitis (a) as described in material and methods. Results are expressed as number of cells per field (#cells/field). The global median of meningoencephalitis group was calculated and employed as a cut off point to discriminate patients with low and high cellularity. Percentages of high cellularity are displayed for virus not detected (undiagnosed) and virus-positive patients with aseptic meningitis. b Virus not detected (undiagnosed) and virus-positive patients with meningoencephalitis were classified as with either high or low cellularity and subdivided in two groups. The levels of the cytokines IL-6, IL-12, IL-17, TNF-α, IFN-γ and IL-10 (expressed as Mean Fluorescence Intensity-MFI) of the subgroups were compared. Statistical differences between subgroups within the same group are highlighted as connecting lines or # and differences between groups (black versus gray) were highlighted as *. The median values for each cytokine measured in the control sample are represented by a dotted line in each graph
Mentions: The cellularity in the CSF was evaluated in patients with meningoencephalitis and healthy controls (Fig. 3). All patients with meningoencephalitis had cellularity above this threshold and controls had cellularity below it. Using the total number of samples, a global median was calculated in order to establish an internal cut off point to differentiate low from high cellularity. Patients with viral meningoencephalitis displayed higher frequency of high cellularity (55 %) when compared with meningoencephalitis patients without viral infection (38 %), however this difference was not statistically significant (Fig. 3a).Fig. 3

Bottom Line: 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).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.

View Article: PubMed Central - PubMed

Affiliation: Tropical Medicine Foundation Dr. Heitor Vieira Dourado, Manaus, AM, Brazil. michelebastos01@gmail.com.

ABSTRACT

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.

No MeSH data available.


Related in: MedlinePlus