Increased neutrophil apoptosis in chronic fatigue syndrome
Background/Aims: Many patients with chronic fatigue syndrome (CFS) have symptoms that are consistent with an underlying viral or toxic illness. Because increased neutrophil apoptosis occurs in patients with infection, this study examined whether this phenomenon also occurs in patients with CFS. Meth...
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| Veröffentlicht in: | Journal of clinical pathology 2004-08, Vol.57 (8), p.891-893 |
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| creator | Kennedy, G Spence, V Underwood, C Belch, J J F |
| description | Background/Aims: Many patients with chronic fatigue syndrome (CFS) have symptoms that are consistent with an underlying viral or toxic illness. Because increased neutrophil apoptosis occurs in patients with infection, this study examined whether this phenomenon also occurs in patients with CFS. Methods: Apoptosis was assessed in patients with CFS in conjunction with concentrations of the anti-inflammatory cytokine, transforming growth factor β1 (TGFβ1). Results: The 47 patients with CFS had higher numbers of apoptotic neutrophils, lower numbers of viable neutrophils, increased annexin V binding, and increased expression of the death receptor, tumour necrosis factor receptor-I, on their neutrophils than did the 34 healthy controls. Patients with CFS also had raised concentrations of active TGFβ1 (p < 0.005). Conclusions: These findings provide new evidence that patients with CFS have an underlying detectable abnormality in their immune cells. |
| doi_str_mv | 10.1136/jcp.2003.015511 |
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Because increased neutrophil apoptosis occurs in patients with infection, this study examined whether this phenomenon also occurs in patients with CFS. Methods: Apoptosis was assessed in patients with CFS in conjunction with concentrations of the anti-inflammatory cytokine, transforming growth factor β1 (TGFβ1). Results: The 47 patients with CFS had higher numbers of apoptotic neutrophils, lower numbers of viable neutrophils, increased annexin V binding, and increased expression of the death receptor, tumour necrosis factor receptor-I, on their neutrophils than did the 34 healthy controls. Patients with CFS also had raised concentrations of active TGFβ1 (p < 0.005). Conclusions: These findings provide new evidence that patients with CFS have an underlying detectable abnormality in their immune cells.</description><identifier>ISSN: 0021-9746</identifier><identifier>EISSN: 1472-4146</identifier><identifier>DOI: 10.1136/jcp.2003.015511</identifier><identifier>PMID: 15280416</identifier><identifier>CODEN: JCPAAK</identifier><language>eng</language><publisher>London: BMJ Publishing Group Ltd and Association of Clinical Pathologists</publisher><subject>Adult ; Annexin A5 - metabolism ; Apoptosis ; Biological and medical sciences ; Biomarkers - analysis ; Blood platelets ; Case-Control Studies ; CFS ; Chronic fatigue syndrome ; Confidence intervals ; Cytokines ; Fatigue Syndrome, Chronic - blood ; Fatigue Syndrome, Chronic - immunology ; Female ; Gangrene ; Growth factors ; Humans ; Illnesses ; Immune system ; Immune System Diseases - complications ; Immune System Diseases - immunology ; Immunity, Cellular ; Immunology ; Infections ; Investigative techniques, diagnostic techniques (general aspects) ; Laboratories ; Male ; Medical sciences ; Middle Aged ; Neutrophils ; Neutrophils - immunology ; Neutrophils - metabolism ; Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques ; platelet poor plasma ; PPP ; propidium iodide ; R&D ; Receptors, Tumor Necrosis Factor - analysis ; Research & development ; Rodents ; Short Report ; TGFβ1 ; TNFRI ; Transforming Growth Factor beta - blood ; transforming growth factor β1 ; Tumor necrosis factor-TNF ; tumour necrosis factor receptor I ; Viral infections</subject><ispartof>Journal of clinical pathology, 2004-08, Vol.57 (8), p.891-893</ispartof><rights>Copyright 2004 Journal of Clinical Pathology</rights><rights>2004 INIST-CNRS</rights><rights>Copyright: 2004 Copyright 2004 Journal of Clinical Pathology</rights><rights>Copyright © Copyright 2004 Journal of Clinical Pathology 2004</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770396/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1770396/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,725,778,782,883,27907,27908,53774,53776</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=16016042$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15280416$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kennedy, G</creatorcontrib><creatorcontrib>Spence, V</creatorcontrib><creatorcontrib>Underwood, C</creatorcontrib><creatorcontrib>Belch, J J F</creatorcontrib><title>Increased neutrophil apoptosis in chronic fatigue syndrome</title><title>Journal of clinical pathology</title><addtitle>J Clin Pathol</addtitle><description>Background/Aims: Many patients with chronic fatigue syndrome (CFS) have symptoms that are consistent with an underlying viral or toxic illness. Because increased neutrophil apoptosis occurs in patients with infection, this study examined whether this phenomenon also occurs in patients with CFS. Methods: Apoptosis was assessed in patients with CFS in conjunction with concentrations of the anti-inflammatory cytokine, transforming growth factor β1 (TGFβ1). Results: The 47 patients with CFS had higher numbers of apoptotic neutrophils, lower numbers of viable neutrophils, increased annexin V binding, and increased expression of the death receptor, tumour necrosis factor receptor-I, on their neutrophils than did the 34 healthy controls. Patients with CFS also had raised concentrations of active TGFβ1 (p < 0.005). Conclusions: These findings provide new evidence that patients with CFS have an underlying detectable abnormality in their immune cells.</description><subject>Adult</subject><subject>Annexin A5 - metabolism</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>Biomarkers - analysis</subject><subject>Blood platelets</subject><subject>Case-Control Studies</subject><subject>CFS</subject><subject>Chronic fatigue syndrome</subject><subject>Confidence intervals</subject><subject>Cytokines</subject><subject>Fatigue Syndrome, Chronic - blood</subject><subject>Fatigue Syndrome, Chronic - immunology</subject><subject>Female</subject><subject>Gangrene</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Illnesses</subject><subject>Immune system</subject><subject>Immune System Diseases - complications</subject><subject>Immune System Diseases - immunology</subject><subject>Immunity, Cellular</subject><subject>Immunology</subject><subject>Infections</subject><subject>Investigative techniques, diagnostic techniques (general aspects)</subject><subject>Laboratories</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neutrophils</subject><subject>Neutrophils - immunology</subject><subject>Neutrophils - metabolism</subject><subject>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</subject><subject>platelet poor plasma</subject><subject>PPP</subject><subject>propidium iodide</subject><subject>R&D</subject><subject>Receptors, Tumor Necrosis Factor - analysis</subject><subject>Research & development</subject><subject>Rodents</subject><subject>Short Report</subject><subject>TGFβ1</subject><subject>TNFRI</subject><subject>Transforming Growth Factor beta - blood</subject><subject>transforming growth factor β1</subject><subject>Tumor necrosis factor-TNF</subject><subject>tumour necrosis factor receptor I</subject><subject>Viral infections</subject><issn>0021-9746</issn><issn>1472-4146</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNpVkU1rGzEQhkVJSdwk597KQuilsK5G39tDoJgmTQkJ9CNXoZW0sVxb2ki7pfn3XWM3aWFgDvPwzDAvQq8BzwGoeL-y_ZxgTOcYOAd4gWbAJKkZMHGAZhgTqBvJxBF6VcoKY6AS6CE6Ak4UZiBm6MNVtNmb4l0V_Tjk1C_DujJ96odUQqlCrOwypxhs1Zkh3I--Ko_R5bTxJ-hlZ9bFn-77Mfpx8en74nN9fXt5tfh4Xbe0oUMNjviGKw6uFQ33naIYOioAOFaCWuVaAqZzlAjFhWmYw02rOmitcxITSegxOt95-7HdeGd9HLJZ6z6HjcmPOpmg_5_EsNT36ZcGKTFtxCQ42wtyehh9GfQqjTlON0-IAkwYZWqi3vy75sn_91cT8HYPmGLNussm2lCeOYGnYtt76x0XyuB_P81N_qmFpJLrm7uF_sK_3TR3Xy_05cS_2_HtZvVsw3obsJ4C1tuA9S5g-gcH_JSr</recordid><startdate>20040801</startdate><enddate>20040801</enddate><creator>Kennedy, G</creator><creator>Spence, V</creator><creator>Underwood, C</creator><creator>Belch, J J F</creator><general>BMJ Publishing Group Ltd and Association of Clinical Pathologists</general><general>BMJ</general><general>BMJ Publishing Group LTD</general><general>Copyright 2004 Journal of Clinical Pathology</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>BTHHO</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>5PM</scope></search><sort><creationdate>20040801</creationdate><title>Increased neutrophil apoptosis in chronic fatigue syndrome</title><author>Kennedy, G ; Spence, V ; Underwood, C ; Belch, J J F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b393t-1d2e95851db695ef8301f361150863c8db21afd326856a94d09b8f1bcdd702723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adult</topic><topic>Annexin A5 - metabolism</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>Biomarkers - analysis</topic><topic>Blood platelets</topic><topic>Case-Control Studies</topic><topic>CFS</topic><topic>Chronic fatigue syndrome</topic><topic>Confidence intervals</topic><topic>Cytokines</topic><topic>Fatigue Syndrome, Chronic - blood</topic><topic>Fatigue Syndrome, Chronic - immunology</topic><topic>Female</topic><topic>Gangrene</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Illnesses</topic><topic>Immune system</topic><topic>Immune System Diseases - complications</topic><topic>Immune System Diseases - immunology</topic><topic>Immunity, Cellular</topic><topic>Immunology</topic><topic>Infections</topic><topic>Investigative techniques, diagnostic techniques (general aspects)</topic><topic>Laboratories</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neutrophils</topic><topic>Neutrophils - immunology</topic><topic>Neutrophils - metabolism</topic><topic>Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques</topic><topic>platelet poor plasma</topic><topic>PPP</topic><topic>propidium iodide</topic><topic>R&D</topic><topic>Receptors, Tumor Necrosis Factor - analysis</topic><topic>Research & development</topic><topic>Rodents</topic><topic>Short Report</topic><topic>TGFβ1</topic><topic>TNFRI</topic><topic>Transforming Growth Factor beta - blood</topic><topic>transforming growth factor β1</topic><topic>Tumor necrosis factor-TNF</topic><topic>tumour necrosis factor receptor I</topic><topic>Viral infections</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kennedy, G</creatorcontrib><creatorcontrib>Spence, V</creatorcontrib><creatorcontrib>Underwood, C</creatorcontrib><creatorcontrib>Belch, J J F</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>BMJ Journals</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database (ProQuest)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of clinical pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kennedy, G</au><au>Spence, V</au><au>Underwood, C</au><au>Belch, J J F</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Increased neutrophil apoptosis in chronic fatigue syndrome</atitle><jtitle>Journal of clinical pathology</jtitle><addtitle>J Clin Pathol</addtitle><date>2004-08-01</date><risdate>2004</risdate><volume>57</volume><issue>8</issue><spage>891</spage><epage>893</epage><pages>891-893</pages><issn>0021-9746</issn><eissn>1472-4146</eissn><coden>JCPAAK</coden><abstract>Background/Aims: Many patients with chronic fatigue syndrome (CFS) have symptoms that are consistent with an underlying viral or toxic illness. Because increased neutrophil apoptosis occurs in patients with infection, this study examined whether this phenomenon also occurs in patients with CFS. Methods: Apoptosis was assessed in patients with CFS in conjunction with concentrations of the anti-inflammatory cytokine, transforming growth factor β1 (TGFβ1). Results: The 47 patients with CFS had higher numbers of apoptotic neutrophils, lower numbers of viable neutrophils, increased annexin V binding, and increased expression of the death receptor, tumour necrosis factor receptor-I, on their neutrophils than did the 34 healthy controls. Patients with CFS also had raised concentrations of active TGFβ1 (p < 0.005). Conclusions: These findings provide new evidence that patients with CFS have an underlying detectable abnormality in their immune cells.</abstract><cop>London</cop><pub>BMJ Publishing Group Ltd and Association of Clinical Pathologists</pub><pmid>15280416</pmid><doi>10.1136/jcp.2003.015511</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adult Annexin A5 - metabolism Apoptosis Biological and medical sciences Biomarkers - analysis Blood platelets Case-Control Studies CFS Chronic fatigue syndrome Confidence intervals Cytokines Fatigue Syndrome, Chronic - blood Fatigue Syndrome, Chronic - immunology Female Gangrene Growth factors Humans Illnesses Immune system Immune System Diseases - complications Immune System Diseases - immunology Immunity, Cellular Immunology Infections Investigative techniques, diagnostic techniques (general aspects) Laboratories Male Medical sciences Middle Aged Neutrophils Neutrophils - immunology Neutrophils - metabolism Pathology. Cytology. Biochemistry. Spectrometry. Miscellaneous investigative techniques platelet poor plasma PPP propidium iodide R&D Receptors, Tumor Necrosis Factor - analysis Research & development Rodents Short Report TGFβ1 TNFRI Transforming Growth Factor beta - blood transforming growth factor β1 Tumor necrosis factor-TNF tumour necrosis factor receptor I Viral infections |
| title | Increased neutrophil apoptosis in chronic fatigue syndrome |
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