Pulmonary stromal-derived factor-1 expression and effect on neutrophil recruitment during acute lung injury.

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  • Additional Information
    • Source:
      Publisher: American Association of Immunologists Country of Publication: United States NLM ID: 2985117R Publication Model: Print Cited Medium: Print ISSN: 0022-1767 (Print) Linking ISSN: 00221767 NLM ISO Abbreviation: J Immunol Subsets: MEDLINE
    • Publication Information:
      Publication: Bethesda, MD : American Association of Immunologists
      Original Publication: Baltimore : Williams & Wilkins, c1950-
    • Subject Terms:
      Chemokines, CXC/*metabolism ; Chemotactic Factors/*metabolism ; Lung/*immunology ; Respiratory Distress Syndrome/*immunology; Animals ; Cell Membrane/immunology ; Cell Movement ; Chemokine CXCL12 ; Chemokines, CXC/analysis ; Chemokines, CXC/genetics ; Chemotactic Factors/antagonists & inhibitors ; Chemotactic Factors/genetics ; Epithelium/chemistry ; Epithelium/immunology ; Female ; Humans ; Lipopolysaccharides/toxicity ; Lung/chemistry ; Lung/drug effects ; Mice ; Mice, Inbred C57BL ; Neutrophils/immunology ; Pneumonia/chemically induced ; Pneumonia/immunology ; RNA, Messenger/analysis ; RNA, Messenger/metabolism ; Receptors, CXCR4/analysis ; Respiratory Distress Syndrome/chemically induced
    • Abstract:
      The severe and protracted inflammation that characterizes acute lung injury (ALI) is driven by the ongoing recruitment of neutrophils to the lung. Although much of the cytokine signaling responsible for the initial phase of ALI has been elaborated, relatively little is known about the mechanisms governing the recruitment of neutrophils from the bone marrow to the lung in the later period of this disease. Given its previously described chemoattractant effects on marrow neutrophils, we investigated whether stromal-derived factor-1 (SDF-1) (CXCL12) might participate in this later phase of recruitment. Using immunohistochemistry to examine both banked human lung specimens from patients with ALI and lungs from mice with LPS-induced pneumonitis, we found that pulmonary SDF-1 expression increases during ALI. We further determined that both lung SDF-1 protein expression and mRNA expression rise in a delayed but sustained pattern in this mouse model and that the major source of the increase in expression appears to be the lung epithelium. Lastly, we found that expression of the SDF-1 receptor CXCR4 rises in a similar temporal pattern on neutrophils in both the blood and airspace of LPS-injured mice and that Ab-mediated SDF-1 blockade significantly attenuates late but not early pulmonary neutrophilia in this model. These results implicate SDF-1 in neutrophil recruitment to the lung in the later period of acute lung injury and suggest a novel role for this cytokine in coordinating the transition from the inflammatory response to the initiation of tissue repair.
    • Grant Information:
      K08 HL 04499 United States HL NHLBI NIH HHS; L30 HL074998 United States HL NHLBI NIH HHS; 1R01 HL 084200 United States HL NHLBI NIH HHS; R01 HL084200 United States HL NHLBI NIH HHS; R01 HL084200-01 United States HL NHLBI NIH HHS
    • Accession Number:
      0 (CXCL12 protein, human)
      0 (CXCR4 protein, mouse)
      0 (Chemokine CXCL12)
      0 (Chemokines, CXC)
      0 (Chemotactic Factors)
      0 (Cxcl12 protein, mouse)
      0 (Lipopolysaccharides)
      0 (RNA, Messenger)
      0 (Receptors, CXCR4)
    • Publication Date:
      Date Created: 20070606 Date Completed: 20070801 Latest Revision: 20220409
    • Publication Date:
      20240829
    • Accession Number:
      10.4049/jimmunol.178.12.8148
    • Accession Number:
      17548653