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Phagocytosis of fossil fuel particulates by macrophages in children with asthma
Abstract Background Airway macrophages clear inhaled soot (black carbon) from traffic fumes. Macrophages from children with asthma have impaired phagocytosis of bacteria, and prostaglandin E2 (PGE2) is associated with impaired phagocytosis by macrophages. We sought to assess whether macrophage phago...
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| Published in: | The Lancet (British edition) 2014-02, Vol.383, p.S29-S29 |
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| creator | Brugha, Rossa, Dr Mushtaq, Naseem, PhD Dundas, Isobel, PhD Mudway, Ian, PhD Sanak, Marek, PhD Grigg, Jonathan, Prof |
| description | Abstract Background Airway macrophages clear inhaled soot (black carbon) from traffic fumes. Macrophages from children with asthma have impaired phagocytosis of bacteria, and prostaglandin E2 (PGE2) is associated with impaired phagocytosis by macrophages. We sought to assess whether macrophage phagocytosis of soot was impaired, and to measure prostanoid metabolites, in children with asthma. Methods In this cross-sectional study, airway macrophages were obtained from 72 children aged 7–14 years by sputum induction with nebulised 4·5% saline. Children were classified as: healthy controls (n=39); mild asthma, defined as British Thoracic Society (BTS) step 1–2 (n=13); or moderate-to-severe asthma (BTS step 3–5) (n=20), and recruited from a UK paediatric outpatient clinic. Healthy controls were recruited as part of the London Low Emission Zone study. Macrophage black carbon was assessed with image analysis by an assessor masked to asthma severity. Exposure to air pollution was calculated by means of the London Air Quality Toolkit. Urinary PGE2 metabolites were measured with high performance liquid chromatography-tandem mass spectrometry. The effect of PGE2 on phagocytosis of black carbon by rat airway macrophages was assessed with an in-vitro phagocytosis assay using urban particulate matter collected from air filters placed at city centre sites in Leicester, UK. Written informed consent was obtained from children and parents (Research Ethics Committee reference 11-LO-1732 and 08/H0704/139). Findings Children with moderate-to-severe asthma had lower airway macrophage black carbon than did controls (median 0·19 mm2 [IQR 0·11–0·26] vs 0·35 [0·16–0·49], p |
| doi_str_mv | 10.1016/S0140-6736(14)60292-0 |
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| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1622605932</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0140673614602920</els_id><sourcerecordid>3229520241</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3500-e2a090a199e1e1e7fab15dcbae970d9528d6d59a5bcaaefd95715f6430bdacfc3</originalsourceid><addsrcrecordid>eNqFkVFrFDEUhYNU6Lb2JxQCvtSHqTczSWbnRZFSq1CooELfwp3MjZuanazJTGX_vdldUehLyUNI-M7h3nMYOxdwKUDot19BSKh02-gLId9oqLu6ghdsIWQrKyXb-yO2-Iccs5OcHwBAalALdvdlhT-i3U4x-8yj4y7m7AN3MwW-wTR5OwecKPN-y9doU9wUQXn6kduVD0Oikf_204pjnlZrfMVeOgyZzv7ep-z7x-tvV5-q27ubz1cfbivbKICKaoQOUHQdiXJah71Qg-2RuhaGTtXLQQ-qQ9VbRHLlpxXKadlAP6B1tjllFwffTYq_ZsqTWftsKQQcKc7ZCF3XZcGuqZ9Hla51q-Ryh75-gj7EOY1lkUKBWEoFrSyUOlAljZwTObNJfo1pawSYXSNm34jZxW2ENPtGDBTd-4OOSjCPnpLJ1tNoafCJ7GSG6J91ePfEwQY_eovhJ20p_x_W5IIfTHYeQu4doPkD0TinsQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1501845074</pqid></control><display><type>article</type><title>Phagocytosis of fossil fuel particulates by macrophages in children with asthma</title><source>Elsevier</source><creator>Brugha, Rossa, Dr ; Mushtaq, Naseem, PhD ; Dundas, Isobel, PhD ; Mudway, Ian, PhD ; Sanak, Marek, PhD ; Grigg, Jonathan, Prof</creator><creatorcontrib>Brugha, Rossa, Dr ; Mushtaq, Naseem, PhD ; Dundas, Isobel, PhD ; Mudway, Ian, PhD ; Sanak, Marek, PhD ; Grigg, Jonathan, Prof</creatorcontrib><description>Abstract Background Airway macrophages clear inhaled soot (black carbon) from traffic fumes. Macrophages from children with asthma have impaired phagocytosis of bacteria, and prostaglandin E2 (PGE2) is associated with impaired phagocytosis by macrophages. We sought to assess whether macrophage phagocytosis of soot was impaired, and to measure prostanoid metabolites, in children with asthma. Methods In this cross-sectional study, airway macrophages were obtained from 72 children aged 7–14 years by sputum induction with nebulised 4·5% saline. Children were classified as: healthy controls (n=39); mild asthma, defined as British Thoracic Society (BTS) step 1–2 (n=13); or moderate-to-severe asthma (BTS step 3–5) (n=20), and recruited from a UK paediatric outpatient clinic. Healthy controls were recruited as part of the London Low Emission Zone study. Macrophage black carbon was assessed with image analysis by an assessor masked to asthma severity. Exposure to air pollution was calculated by means of the London Air Quality Toolkit. Urinary PGE2 metabolites were measured with high performance liquid chromatography-tandem mass spectrometry. The effect of PGE2 on phagocytosis of black carbon by rat airway macrophages was assessed with an in-vitro phagocytosis assay using urban particulate matter collected from air filters placed at city centre sites in Leicester, UK. Written informed consent was obtained from children and parents (Research Ethics Committee reference 11-LO-1732 and 08/H0704/139). Findings Children with moderate-to-severe asthma had lower airway macrophage black carbon than did controls (median 0·19 mm2 [IQR 0·11–0·26] vs 0·35 [0·16–0·49], p<0·0366, Mann-Whitney U test). Airway macrophage black carbon in children with mild asthma was much the same as in controls. Air pollution exposure at the home address did not differ between groups. Moderate to severe asthma was associated with an increase in the urinary PGE2 metabolite, 13,14-dihydro-15-keto-tetranor-PGE2 (median 668 pg/mg creatinine [IQR 293–937] vs 471 [315–623], p<0·05, Mann-Whitney U test). In the 33 children with asthma, this urinary PGE2 metabolite was inversely associated with macrophage carbon (Spearman r =−0·47, p<0·0062). PGE2 suppressed phagocytosis by rat airway macrophages of urban particulate matter to 57% (IQR 41–95) of controls (p<0·0215, Wilcoxon signed rank test). Interpretation Macrophage phagocytosis of black carbon derived from fossil fuel is impaired in moderate-to-severe childhood asthma. This process is associated with raised urinary concentrations of 13,14-dihydro-15-keto-tetranor-PGE2. PGE2 also impairs phagocytosis of black carbon and urban particulate matter by rat airway macrophages in vitro, and is therefore a plausible mediator underlying the impaired phagocytosis seen in macrophages from children with asthma. We now aim to replicate these findings in differentiated human macrophages and to establish airway concentrations of PGE2 from exhaled breath condensate samples taken from these children. Our results suggest a possible mechanism underlying the observation that traffic-derived air pollution adversely affects children with asthma, because they may be less able to clear inhaled particles effectively. Funding Barts and The London Charity.</description><identifier>ISSN: 0140-6736</identifier><identifier>EISSN: 1474-547X</identifier><identifier>DOI: 10.1016/S0140-6736(14)60292-0</identifier><identifier>CODEN: LANCAO</identifier><language>eng</language><publisher>London: Elsevier Ltd</publisher><subject>Air pollution ; Air quality ; Asthma ; Black carbon ; Carbon ; Fossil fuels ; Fumes ; Internal Medicine ; Liquid chromatography ; Mass spectrometry ; Metabolites ; Particulate matter ; Pollution control ; Research ethics ; Soot</subject><ispartof>The Lancet (British edition), 2014-02, Vol.383, p.S29-S29</ispartof><rights>Elsevier Ltd</rights><rights>2014 Elsevier Ltd</rights><rights>Copyright Elsevier Limited Feb 26, 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3500-e2a090a199e1e1e7fab15dcbae970d9528d6d59a5bcaaefd95715f6430bdacfc3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids></links><search><creatorcontrib>Brugha, Rossa, Dr</creatorcontrib><creatorcontrib>Mushtaq, Naseem, PhD</creatorcontrib><creatorcontrib>Dundas, Isobel, PhD</creatorcontrib><creatorcontrib>Mudway, Ian, PhD</creatorcontrib><creatorcontrib>Sanak, Marek, PhD</creatorcontrib><creatorcontrib>Grigg, Jonathan, Prof</creatorcontrib><title>Phagocytosis of fossil fuel particulates by macrophages in children with asthma</title><title>The Lancet (British edition)</title><description>Abstract Background Airway macrophages clear inhaled soot (black carbon) from traffic fumes. Macrophages from children with asthma have impaired phagocytosis of bacteria, and prostaglandin E2 (PGE2) is associated with impaired phagocytosis by macrophages. We sought to assess whether macrophage phagocytosis of soot was impaired, and to measure prostanoid metabolites, in children with asthma. Methods In this cross-sectional study, airway macrophages were obtained from 72 children aged 7–14 years by sputum induction with nebulised 4·5% saline. Children were classified as: healthy controls (n=39); mild asthma, defined as British Thoracic Society (BTS) step 1–2 (n=13); or moderate-to-severe asthma (BTS step 3–5) (n=20), and recruited from a UK paediatric outpatient clinic. Healthy controls were recruited as part of the London Low Emission Zone study. Macrophage black carbon was assessed with image analysis by an assessor masked to asthma severity. Exposure to air pollution was calculated by means of the London Air Quality Toolkit. Urinary PGE2 metabolites were measured with high performance liquid chromatography-tandem mass spectrometry. The effect of PGE2 on phagocytosis of black carbon by rat airway macrophages was assessed with an in-vitro phagocytosis assay using urban particulate matter collected from air filters placed at city centre sites in Leicester, UK. Written informed consent was obtained from children and parents (Research Ethics Committee reference 11-LO-1732 and 08/H0704/139). Findings Children with moderate-to-severe asthma had lower airway macrophage black carbon than did controls (median 0·19 mm2 [IQR 0·11–0·26] vs 0·35 [0·16–0·49], p<0·0366, Mann-Whitney U test). Airway macrophage black carbon in children with mild asthma was much the same as in controls. Air pollution exposure at the home address did not differ between groups. Moderate to severe asthma was associated with an increase in the urinary PGE2 metabolite, 13,14-dihydro-15-keto-tetranor-PGE2 (median 668 pg/mg creatinine [IQR 293–937] vs 471 [315–623], p<0·05, Mann-Whitney U test). In the 33 children with asthma, this urinary PGE2 metabolite was inversely associated with macrophage carbon (Spearman r =−0·47, p<0·0062). PGE2 suppressed phagocytosis by rat airway macrophages of urban particulate matter to 57% (IQR 41–95) of controls (p<0·0215, Wilcoxon signed rank test). Interpretation Macrophage phagocytosis of black carbon derived from fossil fuel is impaired in moderate-to-severe childhood asthma. This process is associated with raised urinary concentrations of 13,14-dihydro-15-keto-tetranor-PGE2. PGE2 also impairs phagocytosis of black carbon and urban particulate matter by rat airway macrophages in vitro, and is therefore a plausible mediator underlying the impaired phagocytosis seen in macrophages from children with asthma. We now aim to replicate these findings in differentiated human macrophages and to establish airway concentrations of PGE2 from exhaled breath condensate samples taken from these children. Our results suggest a possible mechanism underlying the observation that traffic-derived air pollution adversely affects children with asthma, because they may be less able to clear inhaled particles effectively. Funding Barts and The London Charity.</description><subject>Air pollution</subject><subject>Air quality</subject><subject>Asthma</subject><subject>Black carbon</subject><subject>Carbon</subject><subject>Fossil fuels</subject><subject>Fumes</subject><subject>Internal Medicine</subject><subject>Liquid chromatography</subject><subject>Mass spectrometry</subject><subject>Metabolites</subject><subject>Particulate matter</subject><subject>Pollution control</subject><subject>Research ethics</subject><subject>Soot</subject><issn>0140-6736</issn><issn>1474-547X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><recordid>eNqFkVFrFDEUhYNU6Lb2JxQCvtSHqTczSWbnRZFSq1CooELfwp3MjZuanazJTGX_vdldUehLyUNI-M7h3nMYOxdwKUDot19BSKh02-gLId9oqLu6ghdsIWQrKyXb-yO2-Iccs5OcHwBAalALdvdlhT-i3U4x-8yj4y7m7AN3MwW-wTR5OwecKPN-y9doU9wUQXn6kduVD0Oikf_204pjnlZrfMVeOgyZzv7ep-z7x-tvV5-q27ubz1cfbivbKICKaoQOUHQdiXJah71Qg-2RuhaGTtXLQQ-qQ9VbRHLlpxXKadlAP6B1tjllFwffTYq_ZsqTWftsKQQcKc7ZCF3XZcGuqZ9Hla51q-Ryh75-gj7EOY1lkUKBWEoFrSyUOlAljZwTObNJfo1pawSYXSNm34jZxW2ENPtGDBTd-4OOSjCPnpLJ1tNoafCJ7GSG6J91ePfEwQY_eovhJ20p_x_W5IIfTHYeQu4doPkD0TinsQ</recordid><startdate>20140201</startdate><enddate>20140201</enddate><creator>Brugha, Rossa, Dr</creator><creator>Mushtaq, Naseem, PhD</creator><creator>Dundas, Isobel, PhD</creator><creator>Mudway, Ian, PhD</creator><creator>Sanak, Marek, PhD</creator><creator>Grigg, Jonathan, 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of fossil fuel particulates by macrophages in children with asthma</title><author>Brugha, Rossa, Dr ; Mushtaq, Naseem, PhD ; Dundas, Isobel, PhD ; Mudway, Ian, PhD ; Sanak, Marek, PhD ; Grigg, Jonathan, Prof</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3500-e2a090a199e1e1e7fab15dcbae970d9528d6d59a5bcaaefd95715f6430bdacfc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Air pollution</topic><topic>Air quality</topic><topic>Asthma</topic><topic>Black carbon</topic><topic>Carbon</topic><topic>Fossil fuels</topic><topic>Fumes</topic><topic>Internal Medicine</topic><topic>Liquid chromatography</topic><topic>Mass spectrometry</topic><topic>Metabolites</topic><topic>Particulate matter</topic><topic>Pollution control</topic><topic>Research ethics</topic><topic>Soot</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Brugha, Rossa, 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edition)</jtitle><date>2014-02-01</date><risdate>2014</risdate><volume>383</volume><spage>S29</spage><epage>S29</epage><pages>S29-S29</pages><issn>0140-6736</issn><eissn>1474-547X</eissn><coden>LANCAO</coden><abstract>Abstract Background Airway macrophages clear inhaled soot (black carbon) from traffic fumes. Macrophages from children with asthma have impaired phagocytosis of bacteria, and prostaglandin E2 (PGE2) is associated with impaired phagocytosis by macrophages. We sought to assess whether macrophage phagocytosis of soot was impaired, and to measure prostanoid metabolites, in children with asthma. Methods In this cross-sectional study, airway macrophages were obtained from 72 children aged 7–14 years by sputum induction with nebulised 4·5% saline. Children were classified as: healthy controls (n=39); mild asthma, defined as British Thoracic Society (BTS) step 1–2 (n=13); or moderate-to-severe asthma (BTS step 3–5) (n=20), and recruited from a UK paediatric outpatient clinic. Healthy controls were recruited as part of the London Low Emission Zone study. Macrophage black carbon was assessed with image analysis by an assessor masked to asthma severity. Exposure to air pollution was calculated by means of the London Air Quality Toolkit. Urinary PGE2 metabolites were measured with high performance liquid chromatography-tandem mass spectrometry. The effect of PGE2 on phagocytosis of black carbon by rat airway macrophages was assessed with an in-vitro phagocytosis assay using urban particulate matter collected from air filters placed at city centre sites in Leicester, UK. Written informed consent was obtained from children and parents (Research Ethics Committee reference 11-LO-1732 and 08/H0704/139). Findings Children with moderate-to-severe asthma had lower airway macrophage black carbon than did controls (median 0·19 mm2 [IQR 0·11–0·26] vs 0·35 [0·16–0·49], p<0·0366, Mann-Whitney U test). Airway macrophage black carbon in children with mild asthma was much the same as in controls. Air pollution exposure at the home address did not differ between groups. Moderate to severe asthma was associated with an increase in the urinary PGE2 metabolite, 13,14-dihydro-15-keto-tetranor-PGE2 (median 668 pg/mg creatinine [IQR 293–937] vs 471 [315–623], p<0·05, Mann-Whitney U test). In the 33 children with asthma, this urinary PGE2 metabolite was inversely associated with macrophage carbon (Spearman r =−0·47, p<0·0062). PGE2 suppressed phagocytosis by rat airway macrophages of urban particulate matter to 57% (IQR 41–95) of controls (p<0·0215, Wilcoxon signed rank test). Interpretation Macrophage phagocytosis of black carbon derived from fossil fuel is impaired in moderate-to-severe childhood asthma. This process is associated with raised urinary concentrations of 13,14-dihydro-15-keto-tetranor-PGE2. PGE2 also impairs phagocytosis of black carbon and urban particulate matter by rat airway macrophages in vitro, and is therefore a plausible mediator underlying the impaired phagocytosis seen in macrophages from children with asthma. We now aim to replicate these findings in differentiated human macrophages and to establish airway concentrations of PGE2 from exhaled breath condensate samples taken from these children. Our results suggest a possible mechanism underlying the observation that traffic-derived air pollution adversely affects children with asthma, because they may be less able to clear inhaled particles effectively. Funding Barts and The London Charity.</abstract><cop>London</cop><pub>Elsevier Ltd</pub><doi>10.1016/S0140-6736(14)60292-0</doi><oa>free_for_read</oa></addata></record> |
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| subjects | Air pollution Air quality Asthma Black carbon Carbon Fossil fuels Fumes Internal Medicine Liquid chromatography Mass spectrometry Metabolites Particulate matter Pollution control Research ethics Soot |
| title | Phagocytosis of fossil fuel particulates by macrophages in children with asthma |
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