Interleukin-6 released in human cerebrospinal fluid following traumatic brain injury may trigger nerve growth factor production in astrocytes

Kossmann, Thomas; Hans, Volkmar; Imhof, Hans-Georg; Trentz, O.; Morganti-Kossmann, Maria Cristina

doi:10.1016/0006-8993(95)01501-9

Cited by 216 publications

(110 citation statements)

References 50 publications

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“…Enhanced immunoreactivity of splenic NGF in SCID mice and its reduction by T cell transfer suggest that T cells might negatively regulate NGF expression in the spleen. IL-6 has been reported to exert a neurotrophic effect on catecholaminergic and other neurons with or without synergism with NGF (54 -56), and to stimulate NGF production (57,58). We also reported that IL-6, in addition to IL-3, stimulated neurons in nematode-infected lymphoid tissues, as described above (12).…”

Section: Discussionsupporting

confidence: 69%

Neuritogenic Effects of T Cell-Derived IL-3 on Mouse Splenic Sympathetic Neurons In Vivo

Kannan-Hayashi

Okamura

Hattori

et al. 2008

The Journal of Immunology

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To determine the role played by lymphocytes and cytokines in the growth of sympathetic neurons in vivo, the innervation and cytokine levels were examined in the spleens of SCID mice that lack T and B cells. Splenic noradrenaline, nerve growth factor (NGF), and IL-1β levels were elevated in SCID mice. Immunohistochemical examination revealed that the density of tyrosine hydroxylase-positive (TH+) fibers of splenic central arteries in SCID mice was increased compared with wild-type C.B-17 mice, while SCID mice had significantly fewer TH+ fibers in their periarteriolar lymphatic sheaths (PALS). Two weeks after SCID mice were injected with C.B-17 splenic T cells, their TH+ fiber staining increased in the PALS. IL-3 levels increased significantly in SCID mice following T cell reconstitution, and the administration of anti-IL-3 Ab blocked the above T cell-induced increase in innervation in the PALS. Anti-IL-3 treatment also inhibited the regeneration of splenic sympathetic neurons in C.B-17 mice after they were chemically sympathetomized with 6-hydroxydopamine. Depletion of NK cells by anti-asialo GM1 promoted the splenic innervation in SCID mice, while there were no significant changes in the innervation between CD8+ T cell-deficient β2-microglobulin knockout mice and their wild type. Our results suggest that T cells (probably CD4+ Th cells but not CD8+ CTLs) play a role in regulating the sympathetic innervation of the spleen; this effect appeared to be mediated, at least in part, by IL-3. On the contrary, NK cells may exert an inhibitory effect on the sympathetic innervation.

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Section: Discussionsupporting

confidence: 69%

Neuritogenic Effects of T Cell-Derived IL-3 on Mouse Splenic Sympathetic Neurons In Vivo

Kannan-Hayashi

Okamura

Hattori

et al. 2008

The Journal of Immunology

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“…The CSF levels of IL-6 reach a maximum between days 3 and 6 in TBI subjects, 56 with the severity of injury being related to the degree of intracranial IL-6 gradient (venous to arterial ratio) at the time of admission. 57 An in vivo microdialysis study has shown that increased parenchymal IL-6 levels correlate with survival and GOS suggesting that IL-6 is an endogenous neuroprotective cytokine.…”

Section: Interleukin-6mentioning

confidence: 98%

Biomarkers for the Diagnosis, Prognosis, and Evaluation of Treatment Efficacy for Traumatic Brain Injury

et al. 2010

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“…IL-6 is the cytokine found in the highest concentration in human CSF [171]. Measurements in a TBI population displayed maximal levels of IL-6 in the CSF between 3 and 6 days, with a steady decline in release thereafter [173].…”

Section: Human Studies Of T/hsmentioning

confidence: 99%

The Acute Inflammatory Response in Trauma /Hemorrhage and Traumatic Brain Injury: Current State and Emerging Prospects

Namas¹,

Ghuma²,

Hermus

et al. 2008

Libyan Journal of Medicine

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Abstract; Traumatic injury/hemorrhagic shock (T/HS) elicits an acute inflammatory response that may result in death. Inflammation describes a coordinated series of molecular, cellular, tissue, organ, and systemic responses that drive the pathology of various diseases including T/HS and traumatic brain injury (TBI). Inflammation is a finely tuned, dynamic, highly-regulated process that is not inherently detrimental, but rather required for immune surveillance, optimal post-injury tissue repair, and regeneration. The inflammatory response is driven by cytokines and chemokines and is partially propagated by damaged tissue-derived products (Damage-associated Molecular Patterns; DAMP's). DAMPs perpetuate inflammation through the release of pro-inflammatory cytokines, but may also inhibit anti-inflammatory cytokines. Various animal models of T/HS in mice, rats, pigs, dogs, and non-human primates have been utilized in an attempt to move from bench to bedside. Novel approaches, including those from the field of systems biology, may yield therapeutic breakthroughs in T/HS and TBI in the near future.

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Interleukin-6 released in human cerebrospinal fluid following traumatic brain injury may trigger nerve growth factor production in astrocytes

Cited by 216 publications

References 50 publications

Neuritogenic Effects of T Cell-Derived IL-3 on Mouse Splenic Sympathetic Neurons In Vivo

Neuritogenic Effects of T Cell-Derived IL-3 on Mouse Splenic Sympathetic Neurons In Vivo

Biomarkers for the Diagnosis, Prognosis, and Evaluation of Treatment Efficacy for Traumatic Brain Injury

The Acute Inflammatory Response in Trauma /Hemorrhage and Traumatic Brain Injury: Current State and Emerging Prospects

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