Biomedical subjects

E Tarkowski

Publications and source records attributed to E Tarkowski.

At least 19 recordsLinked to original sources

PubMed2004

Increased intrathecal inflammatory activity in frontotemporal dementia: pathophysiological implications.

OBJECTIVE: Immunological mechanisms may be part of the pathophysiological mechanisms in frontotemporal dementia (FTD), but hitherto only vague evidence of such mechanisms has been presented. The aim of this study was to compare the cerebrospinal fluid (CSF) levels of the pro-inflammatory cytokines interleukin (IL)-1beta and tumour necrosis factor (TNF)-alpha, and the anti-inflammatory cytokine transforming growth factor (TGF)-beta in patients with FTD and normal controls. Furthermore, serum levels of TNF-alpha, TGF-beta, and IL-1beta were measured in FTD patients. METHODS: The CSF levels of IL-1beta, TNFalpha, and TGF-beta were measured using ELISA in 19 patients with FTD and 24 sex and age matched healthy controls. RESULTS: The CSF levels of TNF-alpha (FTD 0.6 pg/mL (median: lower, upper quartile 0.3, 0.7); controls: 0.0 pg/mL (0.0, 0.0); p = 0.008) and TGF-beta (FTD 266 pg/mL (157, 371), controls: 147 pg/mL (119, 156); p = 0.0001) were significantly increased in FTD patients compared with controls. No correlations were found between CSF and serum levels of the cytokines. In the controls, but not in the FTD patients, a positive correlation was found between the CSF levels of TGF-beta and age (r = 0.42, p < 0.05). No correlation was found between any of the cytokines and degree of brain atrophy or white matter changes. No differences between the groups were found for age, gender, or CSF/serum albumin ratio. CONCLUSIONS: The results suggest an increased intrathecal production of both pro- and anti-inflammatory cytokines in FTD. As no correlations were found with the albumin ratio, and no correlations between CSF and serum levels of the cytokines were found, these changes in the CSF cannot be explained by a systemic overproduction of cytokines.

Aged↗

PubMed2003

Normal pressure hydrocephalus triggers intrathecal production of TNF-alpha.

Normal pressure hydrocephalus (NPH) is associated with periventricular white matter lesions and demyelination. The aim of the present study was to examine the cerebrospinal fluid (CSF) levels of tumor necrosis factor-alpha (TNF-alpha), a proinflammatory cytokine mediating myelin damage, in patients with NPH. TNF-alpha levels were analyzed by ELISA and measured before and after shunt operation in 35 patients with NPH. The levels of this cytokine were related to the symptomatology and to magnetic resonance imaging (MRI) verified white matter lesions. They were also related to intrathecal levels of sulfatide, a marker for white matter degradation and to levels of neurofilament, a marker for neuronal degeneration. The preoperative levels of TNF-alpha were increased in the CSF of NPH patients compared to controls, and correlated to the levels of sulfatide. The intrathecal TNF-alpha levels were higher in NPH patients with impairment of wakefulness than in those without this symptom. The preoperative TNF-alpha levels were significantly correlated to the improvement of psychometrical test scores, and of wakefulness and to the overall improvement of the patients following shunt operation. Importantly, shunt operation led to complete disappearance of intrathecal TNF-alpha. We conclude that NPH is correlated with intrathecal TNF-alpha production being reversed following shunt operation in parallel with the clinical improvement. The positive correlation between preoperative TNF-alpha and sulfatide levels in the CSF suggest that intrathecal TNF-alpha may contribute to the damage of the white matter known to occur in patients with NPH.

Adult↗

PubMed2003

Intrathecal inflammation precedes development of Alzheimer's disease.

OBJECTIVES: To analyse the cerebrospinal fluid (CSF) values of the proinflammatory cytokines, interleukin 1beta (IL1beta), tumour necrosis factor alpha (TNFalpha), GM-CSF, of the anti-inflammatory cytokine TGFbeta, of tau protein, a marker for neurodegeneration, and of beta amyloid (Abeta), a protein involved in the formation of senile plaques, in prospectively followed up patients with mild cognitive impairment (MCI). METHODS: Analyses of CSF levels of TNFalpha, IL1beta, GM-CSF, TGFbeta, betaa, and tau protein were performed using ELISA in 56 patients with MCI who were followed up prospectively and in 25 age matched, healthy controls. RESULTS: Patients with MCI displayed significantly higher levels of TNFalpha and tau protein and significantly lower levels of TGFbeta and Abeta compared with the healthy controls. After nine months of follow up, 25 patients still displayed MCI while the remaining 31 patients had progressed to Alzheimer's disease (AD). Only MCI patients who progressed to AD at follow up, showed significantly higher CSF levels of TNFalpha than controls. In addition, reduced CSF-Abeta42 levels were only found in MCI patients that progressed to AD, further supporting the notion that disturbed metabolism of Abeta is an early finding in AD. CONCLUSIONS: These results demonstrate increased production of the proinflammatory cytokine, TNFalpha and decreased production of the anti-inflammatory cytokine TGFbeta in patients with MCI at risk to develop AD, suggesting a propensity towards inflammation in this patient group and indicating that CNS inflammation is a early hallmark in the pathogenesis of AD.

Aged↗

PubMed2003

Correlation between intrathecal sulfatide and TNF-alpha levels in patients with vascular dementia.

OBJECTIVES: Subcortical vascular dementia (SVD) is associated with white matter lesions and demyelination. The aim of the present study was to examine the cerebrospinal fluid (CSF) levels of TNF-alpha, a proinflammatory cytokine mediating myelin damage, in SVD patients. The intrathecal TNF-alpha levels were related to the clinical symptoms of dementia, as well as to intrathecal levels of sulfatide, a marker of white matter degradation, and of neurofilament, a marker of neuronal degeneration. METHODS: CSF levels of TNF-a, sulfatide and neurofilament were all analyzed by immunoenzymatic procedures in 17 patients with SVD and in 26 healthy controls. RESULTS: The intrathecal concentration of TNF-alpha was significantly increased in SVD patients compared to healthy controls (p = 0.0001). The intrathecal levels of TNF-alpha were significantly correlated (r = 0.6, p = 0.02) to the levels of sulfatide, but not to the levels of neurofilament, (r = 0.08, NS). CONCLUSIONS: We have demonstrated intrathecal production of TNF-alpha in SVD patients. The correlation between TNF-a and sulfatide levels in the CSF suggests that this apoptosis-inducing cytokine leads to the death of oligodendrocytes, thereby contributing to white matter degeneration, a hallmark of SVD.

Aged↗

PubMed2002

Cytokine response in cerebrospinal fluid from preterm infants with posthaemorrhagic ventricular dilatation.

AIM: Posthaemorrhagic ventricular dilatation (PHVD) is closely associated with white matter damage and neurological disability in the preterm infant. Proinflammatory cytokines have been implicated in the pathogenesis of white matter injury and subsequent cerebral palsy. The aim of this study was to determine the levels of proinflammatory cytokines in cerebrospinal fluid (CSF) from preterm infants with PHVD and to correlate the levels to white matter damage and neurodevelopmental outcome. METHODS: CSF samples were obtained from 24 preterm infants with expanding PHVD and 19 preterm infants with normal ultrasound. Tumour necrosis factor-alphaa (TNF-alpha ), interleukin-1beta (IL-1beta), interleukin-8 (IL-8) and interferon-gamma (IFN-gamma) in CSF were measured by enzyme-linked immunosorbent assay, and IL-6 was measured by bioassay. RESULTS: The concentrations of TNF-alpha, IL-1beta, IL-6 and IL-8 were significantly elevated in CSF from infants with PHVD. TNF-alpha was detected in 43% of PHVD infants and 11% of controls (p = 0.04). IL-1beta was detected in 67% of PHVD infants and 0% of controls (p < 0.0001). The concentrations of IL-6 were 368 (145-460) pg ml(-1) in the PHVD group and 30 (25-41) pg ml(-1) in the control group (p < 0.0001), and those of IL-8 were 3000 (1620-3400) pg ml(-1) in the PHVD group and 35 (0-230) pg ml(-1) in the control group (p < 0.0001). Cytokine concentrations did not correlate with white matter lesions on ultrasound, shunt dependence or neurological outcome within the PHVD group. CONCLUSION: There was an intense and prolonged inflammatory reaction in CSF from preterm infants with PHVD and a high risk for subsequent white matter injury and permanent neurological impairment.

Cerebral Hemorrhage↗

PubMed2001

Local and systemic GM-CSF increase in Alzheimer's disease and vascular dementia.

A growing body of evidence points out the potential role of inflammatory mechanisms in the pathophysiology of brain damage in dementia. The aim of the present study was to investigate patterns of local and systemic cytokine release in patients with Alzheimer's disease (AD) and vascular dementia (VAD). The intrathecal levels of cytokines were related to neuronal damage and cerebral apoptosis. Twenty patients with early AD and 26 patients with VAD were analyzed with respect to cerebrospinal fluid (CSF) and serum levels of pro- and anti-inflammatory cytokines. In addition, CSF levels of Fas/APO-1 and bcl-2, a measure for apoptosis, and Tau protein, a marker for neuronal degradation, were studied. Significantly increased CSF levels of GM-CSF but not of other cytokines were observed in both dementia groups. These patients displayed a significant correlation between the GM-CSF levels and the levels of Fas/APO-1 and Tau protein in CSF. Our study demonstrates an intrathecal production of GM-CSF, a cytokine stimulating microglial cell growth and exerting inflammatogenic properties. It is suggested that GM-CSF once secreted induces programmed cell death in the brain tissue of patients with dementia.

Aged↗

PubMed2000

TNF gene polymorphism and its relation to intracerebral production of TNFalpha and TNFbeta in AD.

OBJECTIVE: To analyze the extent of tumor necrosis factor-alpha (TNFalpha) and TNFbeta gene polymorphism in patients with AD and to relate it to intrathecal levels of these cytokines. METHODS: Analyses of TNFalpha and TNFbeta gene polymorphism were performed using PCR in 52 patients with AD and in 25 control subjects, and the levels of corresponding cytokines were analyzed using ELISA. RESULTS: Patients with AD displayed significantly higher intrathecal levels of TNFalpha, but not TNFbeta, compared with the control subjects. The levels of these cytokines did not differ significantly in patients displaying different alleles of the TNF gene. CONCLUSIONS: Results indicate that increased intrathecal production of TNFalpha in AD is preferentially controlled by environmental stimuli rather than genetic makeup.

Aged↗

PubMed1999

Intracerebral production of tumor necrosis factor-alpha, a local neuroprotective agent, in Alzheimer disease and vascular dementia.

The local pattern of proinflammatory cytokine release was studied in Alzheimer disease (AD) and vascular dementia (VAD), by measuring intrathecal levels of IL-1 beta, IL-6, TNF-alpha, and its naturally occurring antagonists, soluble TNF receptors I and II. The cytokine levels were related to neuronal damage, as measured by the intrathecal tau concentration, to cerebral apoptosis assessed by levels of Fas/APO-1 and bcl-2, and to clinical variables. In vitro analysis was performed to study the effect of TNF-alpha on the production of bcl-2, an antiapoptotic factor, by human neuronal cells. Patients with both AD and VAD displayed significantly higher intrathecal levels of TNF-alpha compared to controls. In addition, patients with AD showed significantly negative correlations between the intrathecal levels of TNF-alpha and the levels of Fas/APO-1 as well as of tau protein. The level of bcl-2 in supernatants of TNF-alpha-exposed cultures of human neuronal cells was up to three times higher than in control supernatants. Our study demonstrates intrathecal production of TNF-alpha in patients with dementias, suggesting that this cytokine may have a neuroprotective role in these neurodegenerative conditions as evidenced by negative correlations between this cytokine and (i) levels of intrathecal Fas/APO-1 and (ii) levels of tau protein, both parameters closely related to brain damage. Our in vitro data suggest that TNF-alpha exerts its neuroprotective effect by stimulating neuronal cells to express bcl-2, a molecule which downregulates apoptosis.

Aged↗

PubMed1999

Intrathecal expression of proteins regulating apoptosis in acute stroke.

BACKGROUND AND PURPOSE: The neuronal death that accompanies an ischemic stroke has previously been attributed to a necrotic process. However, numerous studies in experimental models of ischemia have recently indicated that programmed cell death, also called apoptosis, may contribute to neuronal death. The aim of the present study was to investigate the intrathecal levels of proteins regulating apoptosis in acute stroke and to relate these levels to brain damage and to production of proinflammatory and anti-inflammatory cytokines. METHODS: Thirty stroke patients were studied prospectively on days 0 to 4, 7 to 9, 21 to 26, and after day 90 with clinical evaluation, radiological assessment, and analysis of cerebrospinal fluid (CSF) levels of soluble (s) Fas/APO-1 and sbcl-2, 2 proteins that regulate apoptosis. In addition, analysis of the intrathecal levels of cytokines interleukin (IL)-1beta, IL-6, IL-8, IL-10, granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor-alpha was performed. Nineteen CSF samples from healthy subjects were used for control purposes. The patients were examined with MRI 1 to 3 months after stroke onset for measurement of infarct volume RESULTS: Significantly decreased CSF levels of sFas/APO-1 were observed during the entire observation period, with a maximal decrease on day 21 after the onset of stroke. The intrathecal levels of sFas/APO-1 were significantly negatively correlated with the volume of brain infarct and with the neurological deficit 3 weeks and 3 months after the onset of the stroke. In addition, the intrathecal levels of sFas/APO-1 were significantly correlated with the levels of IL-1beta, IL-6, IL-10, and GM-CSF 3 weeks after the onset of the disease. The intrathecal levels of sbcl-2 were significantly decreased during the first 3 days after stroke onset and at the same time were positively correlated with the levels of IL-6 and tumor necrosis factor-alpha. CONCLUSIONS: Our study demonstrates decreased intrathecal levels of proteins with antiapoptotic properties, suggesting that patients with acute stroke display a propensity toward apoptosis. Control of factors regulating apoptosis may lead to decreased delayed brain damage in stroke.

Acute Disease↗

PubMed1998

Localization of the brain lesion affects the lateralization of T-lymphocyte dependent cutaneous inflammation. Evidence for an immunoregulatory role of the right frontal cortex-putamen region.

We have previously demonstrated that brain lesions caused by stroke led to the lateralization of T-cell dependent inflammation. The purpose of this study was to assess the impact of localization of the brain lesion on lateralization of immune responsiveness. The delayed-type hypersensitivity (DTH) reaction was used as an in vivo measure of antigen specific T-lymphocyte reactivity. All stroke patients were examined with computed scan tomography (CT) of the brain to ascertain the localization and extent of the brain lesion. Patients with right-sided brain lesions displayed significantly larger (P = 0.008) DTH responses on the paretic side compared to the contralateral side. Detailed analysis of the localization of the brain lesion revealed that infarcts encompassing frontal lobe-putamen led to significantly larger (P = 0.007) DTH responses on the paretic side compared to the contralateral side. Localization of the brain lesion affects the lateralization of DTH, supporting an asymmetrical modulation of the immune response. In addition, our study points to the frontal cortex-putamen as a putative brain centre regulating the magnitude of immune responses.

Adult↗

PubMed1998

Cytokine response in cerebrospinal fluid after birth asphyxia.

Experimental studies suggest that cytokine-mediated inflammatory reactions are important in the cascade leading to hypoxic-ischemic brain injury. The purpose was to study the content of pro- and antiinflammatory cytokines in cerebrospinal fluid (CSF) of asphyxiated and control infants. Samples of CSF were obtained from 20 infants who fulfilled the criteria of birth asphyxia and from seven newborn control subjects. The concentrations of IL-1beta, IL-8, IL-10, tumor necrosis factor (TNF)-alpha, and granulocyte/monocyte colony-stimulating factor (GM-CSF) were determined with ELISA and of IL-6 using a bioassay. The concentration of IL-6 (pg/mL) was higher in asphyxiated (250, 35-543; median, interquartile range) than in control (0, 0-18) infants (p = 0.001). There was also a significant relationship between IL-6 and the degree of HIE, and between IL-6 and outcome. In addition, the content of IL-8 (pg/mL) was higher (p = 0.009) in the asphyxia group (170, 70-1440), than in the the control group (10, 0-30) and there was an association between IL-8 and degree of HIE. The levels of IL-10, TNF-alpha, GM-CSF, and IL-1beta did not differ between groups. In conclusion, the proinflammatory cytokines IL-6 and IL-8 were markedly elevated in CSF of asphyxiated infants, and the intrathecal levels of these cytokines corresponded to the degree of HIE.

Apgar Score↗

PubMed1997

Intrathecal release of pro- and anti-inflammatory cytokines during stroke.

A growing body of evidence points out the potential role of inflammatory mechanisms in the pathophysiology of ischaemic brain damage. We have recently demonstrated that stroke patients display an intrathecal production of proinflammatory cytokines, such as IL-1beta and IL-6 already within the first 24 h after the beginning of symptoms (Tarkowski et al., 1995). The aim of the present study was to investigate patterns of local inflammatory responses as a consequence of acute stroke. Thirty stroke patients were studied prospectively on days 0-3, 7-9, 21-26 and after day 90 with clinical evaluations, radiological assessments and analysis of cerebrospinal fluid (CSF) cytokine levels. In addition, 15 healthy control CSF samples were used. Significantly increased CSF levels of IL-8, granulocyte-macrophage colony-stimulating factor (GM-CSF) and IL-10 were observed early during the stroke with a peak on day 2 for the proinflammatory cytokines IL-8 and GM-CSF, and on day 3 for the immunoregulatory cytokine IL-10. Patients with a brain infarct predominantly located in the white matter showed significantly higher levels of IL-8 in CSF than patients with an infarct mainly located in the grey matter. Also, high levels of intrathecal tumour necrosis factor-alpha (TNF-alpha) were associated with the presence of white matter disease. Our study demonstrates an intrathecal production of proinflammatory and immunoregulatory cytokines in patients with stroke, supporting the notion of localized immune response to the acute brain lesion. A better understanding of the inflammatory response in stroke may lead to new treatment strategies.

Adult↗

PubMed1996

Lateralization of cutaneous inflammatory responses in patients with unilateral paresis after poliomyelitis.

Unilateral paresis remaining after poliomyelitis may affect the expression of inflammatory diseases by lateralization of the disease manifestations. The purpose of this study was to assess the impact of the unilateral paresis after poliomyelitis on lateralization of neurogenic inflammation and immune responsiveness. The delayed-type hypersensitivity (DTH) reaction to tuberculin was used as an in vivo measure of antigen-specific T lymphocyte reactivity. Assessment of axon reflex vasodilatation was simultaneously employed to test for neurogenic inflammation. Fourteen of the 16 polio patients displayed a positive DTH reaction to tuberculin. All but two showed weaker DTH reaction on the paretic- compared to the contralateral-side (P = 0.001). Magnitude of electrically evoked axon reflexes significantly correlated to asymmetries of DTH responses. We conclude that damage of lower motor neuron leads to ipsilateral down-regulation of T cell-mediated cutaneous inflammation. This lateralization of DTH responses is related to deficiencies in motor and sympathetic innervation of the paretic extremity.

Adult↗

PubMed1995

Lateralization of T-lymphocyte responses in patients with stroke. Effect of sympathetic dysfunction?

BACKGROUND AND PURPOSE: A number of clinical observations indicate that stroke affects the course of immune-mediated diseases by lateralization of the disease manifestations, such as arthritis. The purpose of this study was to assess the impact of early stroke on lateralization of immune responsiveness. METHODS: The delayed-type hypersensitivity (DTH) reaction to purified protein derivative was used as an in vivo measure of antigen-specific T-lymphocyte reactivity. Assessment of axon reflex vasodilation was simultaneously used to test for cutaneous sympathetic activity. RESULTS: There were no significant differences with regard to lateralization of DTH reactivity when all stroke patients were tested. However, patients with minor stroke displayed a significant (P < .001) decrease of DTH reaction on the paretic side compared with the contralateral side. In contrast, patients with major stroke showed a significant increase (P = .022) of DTH reaction on the paretic side. Patients with left hemiparesis had a significantly greater (P = .045) DTH response on the affected side than patients with a right hemiparesis. In addition, only the patients with motor deficit but not with sensory deficit or aphasia displayed side differences in DTH responses. When electrically evoked axon reflexes were studied in relation to DTH reactions, a significant correlation (r = .64; P < .001) was found between side asymmetries of DTH responses and side asymmetries of axon reflexes in an innervated skin area. No similar relation was present in skin areas where cutaneous sympathetic activity had been blocked by regional anesthesia. CONCLUSIONS: Early stroke lateralizes T-cell-mediated cutaneous inflammation. This effect depends on (1) the localization of the brain lesion, (2) the clinical course of the disease, and (3) the presence of motor deficit and may be mediated by (4) alteration of the cutaneous sympathetic nerve traffic.

Adolescent↗

PubMed1995

Early intrathecal production of interleukin-6 predicts the size of brain lesion in stroke.

BACKGROUND AND PURPOSE: We have previously demonstrated that stroke influences systemic immune responses. The aim of the present study was to investigate patterns of local inflammatory response as a consequence of acute stroke. METHODS: Thirty stroke patients were studied prospectively on days 0 to 3, 7 to 9, 21 to 26, and after day 90 with clinical evaluations, radiological assessments, and analysis of serum and cerebrospinal fluid cytokine levels. RESULTS: Significantly increased levels of interleukin-6 (IL-6) in cerebrospinal fluid (P < .001) were observed in virtually all patients studied compared with healthy control subjects. This increase was observed during the whole observation period but was significantly more pronounced within the first days after stroke onset, with a peak level on days 2 and 3. This initial increase was significantly correlated (r = .65, P = .002) with the volume of infarct measured by MRI 2 to 3 months later. Serum levels of IL-6 in stroke patients were significantly lower than cerebrospinal fluid levels of IL-6 (P = .013) and did not display any significant correlation to the size of the brain lesion. Also, increase in intrathecal but not systemic production of IL-1 beta was observed early during the stroke. Only minor increases of cerebrospinal fluid interferon-gamma levels were observed in two patients. CONCLUSIONS: Our study demonstrates an intrathecal production of IL-6 and IL-1 beta in patients with stroke, supporting the notion of localized inflammatory response to acute brain lesion. In addition, the significant correlation between early intrathecal production of IL-6 and the subsequent size of the brain lesion can be used as a prognostic tool, predicting the size of the brain damage before it is possible to accurately visualize it with radiological methods.

Adult↗

PubMed1995

Stroke induced lateralization of delayed-type hypersensitivity in the early and chronic phase of the disease: a prospective study.

The impact of the acute and chronic phase of stroke on in vivo mediated immune functions was prospectively analysed in patients with mono- and multifocal brain lesions. The cutaneous delayed-type hypersensitivity (DTH) reaction to purified protein derivate was used as an in vivo measure of antigen specific T cell reactivity. Stroke patients have been tested prospectively for DTH reactivity at two separate occasions, 6-12 months apart. Both sides of the body were tested at each occasion. The DTH response on the paretic side changed significantly with time, from being smaller on the paretic side as compared with the contralateral one early after the onset of stroke, to become significantly larger (p = 0.017) in the chronic phase of the disease. In addition, stroke patients showed a significantly larger (p = 0.001) DTH reactivity bilaterally in the chronic phase of the stroke than in the early phase. When patients with single brain lesion and multiple brain lesions were analyzed separately, the increase of DTH reactivity on the paretic side between the 2 challenges was significant (p = 0.016) only in patients with the monofocal disease. We conclude that stroke induces i. an inhibition of DTH reactivity on the paretic side as compared with the non-paretic one in the acute phase but a lateralized enhancement of the DTH reactivity in the chronic phase of the disease, ii. a systemic increase of DTH reactivity in the chronic phase of the disease. Clinical factors positively correlated with these aberrations are: i. right sided, subcortical brain lesion, ii. paresis associated with impaired sensitivity, iii. minor stroke.

Adult↗

PubMed1991

Enhancement of antigen-specific T-cell reactivity on the affected side in stroke patients.

We have analyzed the impact of stroke with subsequent hemiparesis and sensory loss on in vivo mediated immune functions. The delayed-type hypersensitivity (DTH) reaction to purified protein derivate (PPD, tuberculin) was used as a measure of antigen-specific T-cell reactivity, and subcutaneous immunization with influenza vaccine was employed to evaluate T-cell-dependent B-cell function. Thirty-two of the 50 stroke patients tested displayed positive DTH reaction to PPD. All but two showed equal or stronger DTH reaction on the paretic arm compared to the contralateral side (p less than 0.0001). This stroke-induced enhancement of DTH reactivity was evident in patients with combined motor and sensory deficit as well as in subjects with hemiparesis alone. In contrast, immunization of stroke patients with influenza vaccine, a T-cell-dependent B-cell antigen, raised equal antigen-specific serum IgG, IgA and IgM antibody responses irrespective of side (paretic or not paretic). We conclude that stroke enhances antigen-specific T-cell reactivity on the affected side of the body, and that motor but not sensory deficit seems to be required for this enhancement. Antigen-specific B-cell reactivity was not significantly influenced by the hemiparesis.

Aged↗

PubMed1991

Increased systemic T-lymphocyte reactivity in patients with established stroke.

We have analyzed the impact of stroke with subsequent hemiparesis and sensory loss on systemic in vivo and in vitro mediated immune functions. Delayed-type hypersensitivity (DTH) reaction to purified protein derivate (PPD, tuberculin), evaluated on the non-paretic side, was used as an in vivo measure of systemic antigen specific T-cell reactivity. Subcutaneous immunization with influenza vaccine was employed to analyse T-cell dependent B-cell function. The influence of stroke on T-cell function in vitro was studied by proliferative responses to PPD and Concanavalin A. Twenty five out of 54 (46%) stroke patients tested displayed positive DTH reaction to PPD. In contrast, only 24% of age matched controls displayed positive DTH reaction (p < 0.05). There was a good correlation between in vivo and in vitro reactivity to PPD. Consequently, peripheral blood mononuclear cells in 50% of stroke patients but only in 20% of matched controls showed proliferative response in vitro to PPD. Immunization of stroke patients and controls with influenza vaccine, a T-cell dependent B-cell antigen, raised equal antigen-specific serum IgG, IgA and IgM antibody responses in both study groups. We conclude that (a) stroke enhances systemic antigen-specific T-cell reactivity in vivo and in vitro, and (b) stroke has no significant effect on antigen-specific B-cell responses.

Aged↗