{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T00:22:59Z","timestamp":1791073379690,"version":"4.1.0"},"reference-count":26,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2011,10,13]],"date-time":"2011-10-13T00:00:00Z","timestamp":1318464000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["Innate Immun"],"published-print":{"date-parts":[[2012,6]]},"abstract":"<jats:p>Neutrophils are among the first cells to arrive at the site of injury. Chemokines secreted by neutrophils affect the migration of both neutrophils and other inflammatory cells, such as monocytes. It has been reported that LPS-induced release of IL-8 (CXCL-8) by neutrophils is amplified by neutrophil-derived TNF-\u03b1. We hypothesize that chemokine release by neutrophils is altered in chronic obstructive pulmonary disease (COPD) compared with healthy controls and that TNF-\u03b1 may be involved in this alteration. Peripheral blood neutrophils isolated from smokers with COPD ( n\u2009=\u200912), smokers without COPD ( n\u2009=\u200912) and healthy, non-smokers ( n\u2009=\u200912) were stimulated with LPS, TNF-\u03b1 or organic dust. Anti-TNF-\u03b1 Ab (infliximab) was used to study the effect of neutrophil-derived TNF-\u03b1. Release of CXCL-8, macrophage inflammatory protein-1 \u03b1 (MIP-1\u03b1, CCL-3), monocyte chemotactic protein-1 (MCP-1, CCL-2) and TNF-\u03b1 was measured. Neutrophils spontaneously released CXCL-8, CCL-2 and CCL-3. Inhibition of TNF-\u03b1 reduced the spontaneous release of CXCL-8 and CCL-3. Stimulation with LPS and organic dust increased the release of CXCL-8 and CCL-3 (but not CCL-2) which was reduced by inhibition of TNF-\u03b1. In the COPD group, inhibition of TNF-\u03b1 failed to inhibit the release of LPS-induced CXCL-8. The role of neutrophils as cytokine and chemokine producers was confirmed. Neutrophil-derived TNF-\u03b1 contributed to the release of chemokines after stimulation with LPS and organic dust, as the response was inhibited by infliximab. In the COPD group, infliximab did not significantly inhibit the release of CXCL-8, suggesting that the role of TNF-\u03b1 is altered in COPD.<\/jats:p>","DOI":"10.1177\/1753425911423270","type":"journal-article","created":{"date-parts":[[2011,10,13]],"date-time":"2011-10-13T23:07:44Z","timestamp":1318547264000},"page":"503-510","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":27,"title":["Chemokine release by neutrophils in chronic obstructive pulmonary disease"],"prefix":"10.1177","volume":"18","author":[{"given":"Kristin","family":"Blidberg","sequence":"first","affiliation":[{"name":"Lung and Allergy Research, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lena","family":"Palmberg","sequence":"additional","affiliation":[{"name":"Lung and Allergy Research, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Barbro","family":"Dahl\u00e9n","sequence":"additional","affiliation":[{"name":"Division of Respiratory Medicine and Allergy, Department of Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ann-Sofie","family":"Lantz","sequence":"additional","affiliation":[{"name":"Division of Respiratory Medicine and Allergy, Department of Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kjell","family":"Larsson","sequence":"additional","affiliation":[{"name":"Lung and Allergy Research, The National Institute of Environmental Medicine, Karolinska Institutet, Stockholm, 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