Humoral and cellular immunity following severe head injury: review and current investigations<sup>‡</sup>

Quattrocchi, Keith B.; Frank, Edmund; Issel, Bernardo W.; Wagner, Franklin C.

doi:10.1080/01616412.1991.11739977

Cited by 43 publications

(29 citation statements)

References 31 publications

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“…To the best of our knowledge, this has never been studied in brain injury patients before. A few studies have investigated effects of severe head injury on T-lymphocytes and found decreased T-helper cell activation, attenuated lymphokine-activated killer cell cytotoxicity, and depression of PHA-induced pro-inflammatory cytokine production (IL-2 and interferon-c; Miller et al, 1991;Quattrocchi et al, 1990Quattrocchi et al, ,1991Quattrocchi et al, ,1992.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Brain Injury on Heart Rate Variability and the Innate Immune Response in Critically Ill Patients

Kox

Vrouwenvelder

Pompe

et al. 2012

Journal of Neurotrauma

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Brain injury and its related increased intracranial pressure (ICP) may lead to increased vagus nerve activity and the subsequent suppression of innate immunity via the cholinergic anti-inflammatory pathway. This may explain the observed increased susceptibility to infection in these patients. In the present study, we investigated the association between brain injury, vagus nerve activity, and innate immunity. We determined heart rate variability (HRV) as a measure of vagus nerve activity, plasma cytokines, and cytokine production of ex vivo lipopolysaccharide-stimulated whole blood in the first 4 days of admission to the neurological intensive care unit (ICU) in 34 patients with various forms of brain damage. HRV, immune parameters, and the correlations between these measures were analyzed in the entire group of patients and in subgroups of patients with conditions associated with high (intracranial hemorrhage [ICH]) and normal ICP (subarachnoid hemorrhage [SAH] with an extraventricular drain alleviating ICP). Healthy volunteers were used for comparison. HRV total spectral power and ex vivo-stimulated cytokine production were severely depressed in patients compared with healthy volunteers (p<0.05). Furthermore, HRV analysis showed that normalized units of high-frequency power (HFnu, corresponding with vagus nerve activity) was higher, and the low-frequency:high-frequency ratio (LF:HF, corresponding with sympathovagal balance) was lower in patients compared to healthy volunteers (p<0.05). HFnu correlated inversely with ex vivo-stimulated tumor necrosis factor-α (TNF-α) production (r=-0.22, p=0.025). The most pronounced suppression of ex vivo-stimulated cytokine production was observed in the ICH group. Furthermore, in ICH patients, HFnu correlated strongly with lower plasma TNF-α levels (r=-0.73, p=0.002). Our data suggest that brain injury, and especially conditions associated with increased ICP, is associated with vagus nerve-mediated immune suppression.

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Section: Discussionmentioning

confidence: 99%

The Effects of Brain Injury on Heart Rate Variability and the Innate Immune Response in Critically Ill Patients

Kox

Vrouwenvelder

Pompe

et al. 2012

Journal of Neurotrauma

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“…The activity of the phagocytic arm of the immune system early after CNS injury seems to be crucial for the appearance of infection and second-hit complications [19][20][21][22].…”

Section: Discussionmentioning

confidence: 99%

Immunomonitoring in patients with early moderate and severe head trauma

Marks¹,

Gołąbek-Dropiewska²,

Bryl³

et al. 2013

cejoi

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“…10 In addition, suppression of cellular immunity, in particular helper T-cell function, has been reported following head injury and surgical trauma, 11,23,24 and is mediated by decreased interleukin-2 and interferon-gamma production 25 as well as lymphocyte dysfunction. 26 Although suppression of cellular immunity would seem to be protective against the development of GBS, in part explaining the infrequent development of GBS following head trauma, it remains possible that head trauma may result in reduction of regulatory T-cell function. Given that a reduction of regulatory Tcells has been reported in GBS, 27 further studies assessing the pathophysiological role of regulatory T-cells in the development of GBS following head trauma may yet prove useful.…”

Section: Discussionmentioning

confidence: 99%

Severe Guillain-Barré syndrome following head trauma

Tan

Vucic

2010

Journal of Clinical Neuroscience

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Humoral and cellular immunity following severe head injury: review and current investigations^‡

Cited by 43 publications

References 31 publications

The Effects of Brain Injury on Heart Rate Variability and the Innate Immune Response in Critically Ill Patients

The Effects of Brain Injury on Heart Rate Variability and the Innate Immune Response in Critically Ill Patients

Immunomonitoring in patients with early moderate and severe head trauma

Severe Guillain-Barré syndrome following head trauma

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Humoral and cellular immunity following severe head injury: review and current investigations‡

Cited by 43 publications

References 31 publications

The Effects of Brain Injury on Heart Rate Variability and the Innate Immune Response in Critically Ill Patients

The Effects of Brain Injury on Heart Rate Variability and the Innate Immune Response in Critically Ill Patients

Immunomonitoring in patients with early moderate and severe head trauma

Severe Guillain-Barré syndrome following head trauma

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Humoral and cellular immunity following severe head injury: review and current investigations^‡