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The reduction in interstitial and airway neutrophil recruitment was not due to a cell-intrinsic migratory defect, because Hck- and Fgr-deficient neutrophils were attracted to the airways by the chemokine CXCL2 as wild type cells. However, early accumulation of chemokines and TNF-\u03b1 in the airways was reduced in hck\u2212\/\u2212fgr\u2212\/\u2212 mice. Considering that chemokine and TNF-\u03b1 release into the airways was neutrophil independent, as suggested by a comparison between control and neutrophil-depleted mice, we examined LPS-induced chemokine secretion by neutrophils and macrophages in wild type and mutant cells. Notably, mutant neutrophils displayed a marked deficit in their capability to release the chemokines CXCL1, CXCL2, CCL3, and CCL4 and TNF-\u03b1 in response to LPS. However, intracellular accumulation of these chemokines and TNF-\u03b1, as well as secretion of a wide array of cytokines, including IL-1\u03b1, IL-1\u03b2, IL-6, and IL-10, by hck\u2212\/\u2212fgr\u2212\/\u2212 neutrophils was normal. Intriguingly, secretion of CXCL1, CXCL2, CCL2, CCL3, CCL4, RANTES, and TNF-\u03b1, but not IL-1\u03b1, IL-1\u03b2, IL-6, IL-10, and GM-CSF, was also markedly reduced in bone marrow\u2013derived macrophages. Consistently, the Src kinase inhibitors PP2 and dasatinib reduced chemokine secretion by neutrophils and bone marrow\u2013derived macrophages. These findings identify Src kinases as a critical regulator of chemokine secretion in myeloid leukocytes during lung inflammation.<\/jats:p>","DOI":"10.4049\/jimmunol.1402011","type":"journal-article","created":{"date-parts":[[2015,8,1]],"date-time":"2015-08-01T02:30:11Z","timestamp":1438396211000},"page":"2383-2395","source":"Crossref","is-referenced-by-count":38,"title":["The Src-Family Kinases Hck and Fgr Regulate Early Lipopolysaccharide-Induced Myeloid Cell Recruitment into the Lung and Their Ability To Secrete Chemokines"],"prefix":"10.1093","volume":"195","author":[{"given":"Paola","family":"Mazzi","sequence":"first","affiliation":[{"name":"Section of General Pathology, Department of Pathology and Diagnostics, University of Verona , Verona, 37134 ,","place":["Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elena","family":"Caveggion","sequence":"additional","affiliation":[{"name":"Section of General Pathology, Department of Pathology and Diagnostics, University of Verona , Verona, 37134 ,","place":["Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jos\u00e8 A","family":"Lapinet-Vera","sequence":"additional","affiliation":[{"name":"Section of General Pathology, Department of Pathology and Diagnostics, University of Verona , Verona, 37134 ,","place":["Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Clifford A","family":"Lowell","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine, University of California , San Francisco, San Francisco, CA 94143"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Giorgio","family":"Berton","sequence":"additional","affiliation":[{"name":"Section of General Pathology, Department of Pathology and Diagnostics, University of Verona , Verona, 37134 ,","place":["Italy"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2015,9,1]]},"reference":[{"key":"2025030704083428100_r1","doi-asserted-by":"crossref","first-page":"L665","DOI":"10.1152\/ajplung.00232.2013","article-title":"Novel concepts of acute lung injury and alveolar-capillary barrier dysfunction","volume":"305","author":"Herold","year":"2013","journal-title":"Am. 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