Transient gene transfer of non-ELR chemokines to rodent lung induces mononuclear cell accumulation and activation.

The in vivo function of the CXC chemokines interferon-inducible protein-10 (IP-10) and monokine induced by gamma (MIG) was examined using replication-deficient adenoviral vectors expressing human IP-10 (AdIP-10) or murine MIG (AdMIG). Intratracheal and intranasal administration of AdIP-10 or AdMIG into rats and mice produced transient chemokine overexpression from the bronchial epithelium. IP-10 concentrations in the bronchoalveolar lavage fluid (BAL) of AdIP-10-treated animals showed peak expression (>2 ng/ml) 24-48 h after AdIP-10 administration. Dramatic transient increases in BAL cellularity (macrophages, monocytes, lymphocytes, and neutrophils) were observed in AdIP-10-treated and AdMIG-treated animals, and histologic examination of AdIP-10-treated lungs revealed transient infiltrations of mononuclear cells primarily localized around the bronchus and extending throughout the lung parenchyma. However, in immunocomprised SCID mice, only increases in natural killer cell populations were detected in BAL following AdIP-10 intranasal administration, indicating that monocyte/macrophage and neutrophil accumulation was likely the result of factors released from activated lymphocytes.

[1]  F. Graham,et al.  A double recombinant adenovirus expressing the costimulatory molecule B7-1 (murine) and human IL-2 induces complete tumor regression in a murine breast adenocarcinoma model. , 1998, Journal of immunology.

[2]  M. Baggiolini,et al.  CCR5 is characteristic of Th1 lymphocytes , 1998, Nature.

[3]  P. Allavena,et al.  Differential Expression of Chemokine Receptors and Chemotactic Responsiveness of Type 1 T Helper Cells (Th1s) and Th2s , 1998, The Journal of experimental medicine.

[4]  A. Maghazachi,et al.  Interferon‐inducible protein‐10 and lymphotactin induce the chemotaxis and mobilization of intracellular calcium in natural killer cells through pertussis toxin‐sensitive and ‐insensitive heterotrimeric G‐proteins , 1997, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[5]  J. Farber.  Mig and IP‐10: CXC chemokines that target lymphocytes , 1997, Journal of leukocyte biology.

[6]  T. Schall,et al.  Overexpression of RANTES using a recombinant adenovirus vector induces the tissue-directed recruitment of monocytes to the lung. , 1996, Journal of immunology.

[7]  D. Taub.  Chemokine-leukocyte interactions. The voodoo that they do so well. , 1996, Cytokine & growth factor reviews.

[8]  L. Koniaris,et al.  Interferon-inducible protein-10 identified as a mediator of tumor necrosis in vivo. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[9]  F. Graham,et al.  Adenoviral gene transfer of macrophage inflammatory protein-2 in rat lung. , 1996, The American journal of pathology.

[10]  Simon A. Jones,et al.  Chemokine receptor specific for IP10 and mig: structure, function, and expression in activated T-lymphocytes , 1996, The Journal of experimental medicine.

[11]  R. Whyte,et al.  Interferon-gamma-inducible protein 10 (IP-10) is an angiostatic factor that inhibits human non-small cell lung cancer (NSCLC) tumorigenesis and spontaneous metastases , 1996, The Journal of experimental medicine.

[12]  D. Taub,et al.  Human interferon-inducible protein-10 induces mononuclear cell infiltration in mice and promotes the migration of human T lymphocytes into the peripheral tissues and human peripheral blood lymphocytes-SCID mice. , 1996, Blood.

[13]  M. Baggiolini,et al.  Activation of NK cells by CC chemokines. Chemotaxis, Ca2+ mobilization, and enzyme release. , 1996, Journal of immunology.

[14]  D. Taub,et al.  Alpha and beta chemokines induce NK cell migration and enhance NK-mediated cytolysis. , 1995, Journal of immunology.

[15]  D. Taub,et al.  Human Interferon-inducible Protein 10 Is a Potent Inhibitor of Angiogenesis in Vivo , 1995 .

[16]  M. Burdick,et al.  Interferon gamma-inducible protein 10 (IP-10), a member of the C-X-C chemokine family, is an inhibitor of angiogenesis. , 1995, Biochemical and biophysical research communications.

[17]  M. Jordana,et al.  Adenovirus-mediated cytokine gene transfer at tissue sites. Overexpression of IL-6 induces lymphocytic hyperplasia in the lung. , 1994, Journal of immunology.

[18]  F. Graham,et al.  An efficient and flexible system for construction of adenovirus vectors with insertions or deletions in early regions 1 and 3. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[19]  J. Krueger,et al.  Human interferon-inducible protein 10: expression and purification of recombinant protein demonstrate inhibition of early human hematopoietic progenitors , 1993, The Journal of experimental medicine.

[20]  D. Taub,et al.  Recombinant human interferon-inducible protein 10 is a chemoattractant for human monocytes and T lymphocytes and promotes T cell adhesion to endothelial cells , 1993, The Journal of experimental medicine.

[21]  B. Dewald,et al.  IP-10, a gamma-interferon-inducible protein related to interleukin-8, lacks neutrophil activating properties. , 1992, Immunology letters.

[22]  A. Enk,et al.  Early molecular events in the induction phase of contact sensitivity. , 1992, Proceedings of the National Academy of Sciences of the United States of America.

[23]  A. Gottlieb,et al.  Fixed drug eruptions: evidence for a cytokine‐mediated process , 1991, Journal of cutaneous pathology.

[24]  A. Gottlieb,et al.  Detection of a gamma interferon-induced protein IP-10 in psoriatic plaques , 1988, The Journal of experimental medicine.

[25]  G. Kaplan,et al.  The expression of a gamma interferon-induced protein (IP-10) in delayed immune responses in human skin , 1987, The Journal of experimental medicine.

[26]  Andrew D. Luster,et al.  γ-Interferon transcriptionally regulates an early-response gene containing homology to platelet proteins , 1985, Nature.