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Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress
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| Zeitschriftentitel: | BioMed Research International |
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| Personen und Körperschaften: | , , , , , , |
| In: | BioMed Research International, 2014, 2014, S. 1-6 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Hindawi Limited
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| Schlagwörter: |
| author_facet |
Swardfager, W. Herrmann, N. Andreazza, A. C. Swartz, R. H. Khan, M. M. Black, S. E. Lanctôt, K. L. Swardfager, W. Herrmann, N. Andreazza, A. C. Swartz, R. H. Khan, M. M. Black, S. E. Lanctôt, K. L. |
|---|---|
| author |
Swardfager, W. Herrmann, N. Andreazza, A. C. Swartz, R. H. Khan, M. M. Black, S. E. Lanctôt, K. L. |
| spellingShingle |
Swardfager, W. Herrmann, N. Andreazza, A. C. Swartz, R. H. Khan, M. M. Black, S. E. Lanctôt, K. L. BioMed Research International Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress General Immunology and Microbiology General Biochemistry, Genetics and Molecular Biology General Medicine |
| author_sort |
swardfager, w. |
| spelling |
Swardfager, W. Herrmann, N. Andreazza, A. C. Swartz, R. H. Khan, M. M. Black, S. E. Lanctôt, K. L. 2314-6133 2314-6141 Hindawi Limited General Immunology and Microbiology General Biochemistry, Genetics and Molecular Biology General Medicine http://dx.doi.org/10.1155/2014/245210 <jats:p>Stroke variably activates interleukin- (IL-) 17 expression, reduces regulatory T cells, and induces oxidative stress, which may support neurodegeneration. Ischemic stroke patients were screened for depressive symptoms (Center for Epidemiological Studies Depression (CES-D)) and cognitive status (Mini Mental State Examination). Proinflammatory cytokines (IL-17, IL-23, and interferon- [IFN-]<jats:italic>γ</jats:italic>), anti-inflammatory cytokine IL-10, and lipid hydroperoxide (LPH), a measure of oxidative stress, were assayed from fasting serum. Of 47 subjects (age 71.8 ± 14.4 years, 36% female), 19 had depressive symptoms (CES-D ≥ 16), which was associated with poorer cognitive status (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:msub><mml:mrow><mml:mi>F</mml:mi></mml:mrow><mml:mrow><mml:mn>1,46</mml:mn></mml:mrow></mml:msub><mml:mo>=</mml:mo><mml:mn>8.44</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M2"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.006</mml:mn></mml:math>). IL-17 concentrations did not differ between subjects with and without depressive symptoms (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M3"><mml:msub><mml:mrow><mml:mi>F</mml:mi></mml:mrow><mml:mrow><mml:mn>1,46</mml:mn></mml:mrow></mml:msub><mml:mo>=</mml:mo><mml:mn>8.44</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M4"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.572</mml:mn></mml:math>); however, IL-17 was associated with poorer cognitive status in subjects with depressive symptoms (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M5"><mml:msub><mml:mrow><mml:mi>F</mml:mi></mml:mrow><mml:mrow><mml:mn>1,46</mml:mn></mml:mrow></mml:msub><mml:mo>=</mml:mo><mml:mn>9.29</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M6"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.004</mml:mn></mml:math>). In those subjects with depressive symptoms, IL-17 was associated with higher LPH (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M7"><mml:mi>ρ</mml:mi><mml:mo>=</mml:mo><mml:mn>0.518</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M8"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.023</mml:mn></mml:math>) and lower IL-10 (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M9"><mml:mi>ρ</mml:mi><mml:mo>=</mml:mo><mml:mo>-</mml:mo><mml:mn>0.484</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M10"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.036</mml:mn></mml:math>), but not in those without. In conclusion, poststroke depressive symptoms may be associated with cognitive vulnerability to IL-17 related pathways, involving an imbalance between proinflammatory and anti-inflammatory activity and increased oxidative stress.</jats:p> Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress BioMed Research International |
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10.1155/2014/245210 |
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Hindawi Limited, 2014 |
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Hindawi Limited, 2014 |
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2314-6133 2314-6141 |
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2014 |
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BioMed Research International |
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| title |
Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress |
| title_unstemmed |
Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress |
| title_full |
Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress |
| title_fullStr |
Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress |
| title_full_unstemmed |
Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress |
| title_short |
Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress |
| title_sort |
poststroke neuropsychiatric symptoms: relationships with il-17 and oxidative stress |
| topic |
General Immunology and Microbiology General Biochemistry, Genetics and Molecular Biology General Medicine |
| url |
http://dx.doi.org/10.1155/2014/245210 |
| publishDate |
2014 |
| physical |
1-6 |
| description |
<jats:p>Stroke variably activates interleukin- (IL-) 17 expression, reduces regulatory T cells, and induces oxidative stress, which may support neurodegeneration. Ischemic stroke patients were screened for depressive symptoms (Center for Epidemiological Studies Depression (CES-D)) and cognitive status (Mini Mental State Examination). Proinflammatory cytokines (IL-17, IL-23, and interferon- [IFN-]<jats:italic>γ</jats:italic>), anti-inflammatory cytokine IL-10, and lipid hydroperoxide (LPH), a measure of oxidative stress, were assayed from fasting serum. Of 47 subjects (age 71.8 ± 14.4 years, 36% female), 19 had depressive symptoms (CES-D ≥ 16), which was associated with poorer cognitive status (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:msub><mml:mrow><mml:mi>F</mml:mi></mml:mrow><mml:mrow><mml:mn>1,46</mml:mn></mml:mrow></mml:msub><mml:mo>=</mml:mo><mml:mn>8.44</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M2"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.006</mml:mn></mml:math>). IL-17 concentrations did not differ between subjects with and without depressive symptoms (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M3"><mml:msub><mml:mrow><mml:mi>F</mml:mi></mml:mrow><mml:mrow><mml:mn>1,46</mml:mn></mml:mrow></mml:msub><mml:mo>=</mml:mo><mml:mn>8.44</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M4"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.572</mml:mn></mml:math>); however, IL-17 was associated with poorer cognitive status in subjects with depressive symptoms (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M5"><mml:msub><mml:mrow><mml:mi>F</mml:mi></mml:mrow><mml:mrow><mml:mn>1,46</mml:mn></mml:mrow></mml:msub><mml:mo>=</mml:mo><mml:mn>9.29</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M6"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.004</mml:mn></mml:math>). In those subjects with depressive symptoms, IL-17 was associated with higher LPH (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M7"><mml:mi>ρ</mml:mi><mml:mo>=</mml:mo><mml:mn>0.518</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M8"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.023</mml:mn></mml:math>) and lower IL-10 (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M9"><mml:mi>ρ</mml:mi><mml:mo>=</mml:mo><mml:mo>-</mml:mo><mml:mn>0.484</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M10"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.036</mml:mn></mml:math>), but not in those without. In conclusion, poststroke depressive symptoms may be associated with cognitive vulnerability to IL-17 related pathways, involving an imbalance between proinflammatory and anti-inflammatory activity and increased oxidative stress.</jats:p> |
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| description | <jats:p>Stroke variably activates interleukin- (IL-) 17 expression, reduces regulatory T cells, and induces oxidative stress, which may support neurodegeneration. Ischemic stroke patients were screened for depressive symptoms (Center for Epidemiological Studies Depression (CES-D)) and cognitive status (Mini Mental State Examination). Proinflammatory cytokines (IL-17, IL-23, and interferon- [IFN-]<jats:italic>γ</jats:italic>), anti-inflammatory cytokine IL-10, and lipid hydroperoxide (LPH), a measure of oxidative stress, were assayed from fasting serum. Of 47 subjects (age 71.8 ± 14.4 years, 36% female), 19 had depressive symptoms (CES-D ≥ 16), which was associated with poorer cognitive status (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:msub><mml:mrow><mml:mi>F</mml:mi></mml:mrow><mml:mrow><mml:mn>1,46</mml:mn></mml:mrow></mml:msub><mml:mo>=</mml:mo><mml:mn>8.44</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M2"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.006</mml:mn></mml:math>). IL-17 concentrations did not differ between subjects with and without depressive symptoms (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M3"><mml:msub><mml:mrow><mml:mi>F</mml:mi></mml:mrow><mml:mrow><mml:mn>1,46</mml:mn></mml:mrow></mml:msub><mml:mo>=</mml:mo><mml:mn>8.44</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M4"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.572</mml:mn></mml:math>); however, IL-17 was associated with poorer cognitive status in subjects with depressive symptoms (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M5"><mml:msub><mml:mrow><mml:mi>F</mml:mi></mml:mrow><mml:mrow><mml:mn>1,46</mml:mn></mml:mrow></mml:msub><mml:mo>=</mml:mo><mml:mn>9.29</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M6"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.004</mml:mn></mml:math>). In those subjects with depressive symptoms, IL-17 was associated with higher LPH (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M7"><mml:mi>ρ</mml:mi><mml:mo>=</mml:mo><mml:mn>0.518</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M8"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.023</mml:mn></mml:math>) and lower IL-10 (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M9"><mml:mi>ρ</mml:mi><mml:mo>=</mml:mo><mml:mo>-</mml:mo><mml:mn>0.484</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M10"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.036</mml:mn></mml:math>), but not in those without. In conclusion, poststroke depressive symptoms may be associated with cognitive vulnerability to IL-17 related pathways, involving an imbalance between proinflammatory and anti-inflammatory activity and increased oxidative stress.</jats:p> |
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| spelling | Swardfager, W. Herrmann, N. Andreazza, A. C. Swartz, R. H. Khan, M. M. Black, S. E. Lanctôt, K. L. 2314-6133 2314-6141 Hindawi Limited General Immunology and Microbiology General Biochemistry, Genetics and Molecular Biology General Medicine http://dx.doi.org/10.1155/2014/245210 <jats:p>Stroke variably activates interleukin- (IL-) 17 expression, reduces regulatory T cells, and induces oxidative stress, which may support neurodegeneration. Ischemic stroke patients were screened for depressive symptoms (Center for Epidemiological Studies Depression (CES-D)) and cognitive status (Mini Mental State Examination). Proinflammatory cytokines (IL-17, IL-23, and interferon- [IFN-]<jats:italic>γ</jats:italic>), anti-inflammatory cytokine IL-10, and lipid hydroperoxide (LPH), a measure of oxidative stress, were assayed from fasting serum. Of 47 subjects (age 71.8 ± 14.4 years, 36% female), 19 had depressive symptoms (CES-D ≥ 16), which was associated with poorer cognitive status (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M1"><mml:msub><mml:mrow><mml:mi>F</mml:mi></mml:mrow><mml:mrow><mml:mn>1,46</mml:mn></mml:mrow></mml:msub><mml:mo>=</mml:mo><mml:mn>8.44</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M2"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.006</mml:mn></mml:math>). IL-17 concentrations did not differ between subjects with and without depressive symptoms (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M3"><mml:msub><mml:mrow><mml:mi>F</mml:mi></mml:mrow><mml:mrow><mml:mn>1,46</mml:mn></mml:mrow></mml:msub><mml:mo>=</mml:mo><mml:mn>8.44</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M4"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.572</mml:mn></mml:math>); however, IL-17 was associated with poorer cognitive status in subjects with depressive symptoms (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M5"><mml:msub><mml:mrow><mml:mi>F</mml:mi></mml:mrow><mml:mrow><mml:mn>1,46</mml:mn></mml:mrow></mml:msub><mml:mo>=</mml:mo><mml:mn>9.29</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M6"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.004</mml:mn></mml:math>). In those subjects with depressive symptoms, IL-17 was associated with higher LPH (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M7"><mml:mi>ρ</mml:mi><mml:mo>=</mml:mo><mml:mn>0.518</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M8"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.023</mml:mn></mml:math>) and lower IL-10 (<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M9"><mml:mi>ρ</mml:mi><mml:mo>=</mml:mo><mml:mo>-</mml:mo><mml:mn>0.484</mml:mn></mml:math>,<mml:math xmlns:mml="http://www.w3.org/1998/Math/MathML" id="M10"><mml:mi>P</mml:mi><mml:mo>=</mml:mo><mml:mn>0.036</mml:mn></mml:math>), but not in those without. In conclusion, poststroke depressive symptoms may be associated with cognitive vulnerability to IL-17 related pathways, involving an imbalance between proinflammatory and anti-inflammatory activity and increased oxidative stress.</jats:p> Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress BioMed Research International |
| spellingShingle | Swardfager, W., Herrmann, N., Andreazza, A. C., Swartz, R. H., Khan, M. M., Black, S. E., Lanctôt, K. L., BioMed Research International, Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress, General Immunology and Microbiology, General Biochemistry, Genetics and Molecular Biology, General Medicine |
| title | Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress |
| title_full | Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress |
| title_fullStr | Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress |
| title_full_unstemmed | Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress |
| title_short | Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress |
| title_sort | poststroke neuropsychiatric symptoms: relationships with il-17 and oxidative stress |
| title_unstemmed | Poststroke Neuropsychiatric Symptoms: Relationships with IL-17 and Oxidative Stress |
| topic | General Immunology and Microbiology, General Biochemistry, Genetics and Molecular Biology, General Medicine |
| url | http://dx.doi.org/10.1155/2014/245210 |