tetano
Editor, Senior Moderator
Cytokine. 2012 Jan 23. [Epub ahead of print]
Characterizing antiviral mechanism of interleukin-32 and a circulating soluble isoform in viral infection.
Bae S, Kang D, Hong J, Chung B, Choi J, Jhun H, Hong K, Kim E, Jo S, Lee S, Kim SH, Kim S.
Source
Laboratory of Cytokine Immunology, Department of Biomedical Science and Technology, Konkuk University, Seoul 143-701, Republic of Korea.
Abstract
Interleukin-32 (IL-32) is an inflammatory cytokine, and its activity is associated with various auto-inflammatory disorders as well as infectious pathogens such as Mycobacterium tuberculosis, and viral infections. However, the precise antiviral mechanism of IL-32 remains unclear. We assessed the IL-32 level in the sera of H1N1 influenza A patients and IL-32 level was significantly elevated. Next we examined the antiviral activity of recombinant IL-32γ (rIL-32γ) with WISH cells infected by vesicular stomatitis virus (VSV) but no antiviral activity was observed. Therefore we investigated the supernatant of rIL-32-treated THP-1 cells since this cell line effectively responded to rIL-32γ. The supernatant of rIL-32-treated THP-1 cell possessed an antiviral effect and in addition, an agonistic monoclonal antibody further enhanced a specific antiviral activity of rIL-32γ. The fractionation and mass spectrometer analysis of the THP-1 cell supernatant revealed that the antiviral activity of rIL-32γ is via a THP-1 cell-produced factor, transferrin, rather than the direct effects of rIL-32γ on epithelial cells. We also characterized a secreted soluble IL-32γ protein in serum of IL-32γ transgenic mouse (TG), but not in that of IL-32α TG. The present results suggest that IL-32γ expression and its genetic variation in individual could be an important aspect of viral infections.
Copyright ? 2012 Elsevier Ltd. All rights reserved.
PMID:
22277801
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22277801
Characterizing antiviral mechanism of interleukin-32 and a circulating soluble isoform in viral infection.
Bae S, Kang D, Hong J, Chung B, Choi J, Jhun H, Hong K, Kim E, Jo S, Lee S, Kim SH, Kim S.
Source
Laboratory of Cytokine Immunology, Department of Biomedical Science and Technology, Konkuk University, Seoul 143-701, Republic of Korea.
Abstract
Interleukin-32 (IL-32) is an inflammatory cytokine, and its activity is associated with various auto-inflammatory disorders as well as infectious pathogens such as Mycobacterium tuberculosis, and viral infections. However, the precise antiviral mechanism of IL-32 remains unclear. We assessed the IL-32 level in the sera of H1N1 influenza A patients and IL-32 level was significantly elevated. Next we examined the antiviral activity of recombinant IL-32γ (rIL-32γ) with WISH cells infected by vesicular stomatitis virus (VSV) but no antiviral activity was observed. Therefore we investigated the supernatant of rIL-32-treated THP-1 cells since this cell line effectively responded to rIL-32γ. The supernatant of rIL-32-treated THP-1 cell possessed an antiviral effect and in addition, an agonistic monoclonal antibody further enhanced a specific antiviral activity of rIL-32γ. The fractionation and mass spectrometer analysis of the THP-1 cell supernatant revealed that the antiviral activity of rIL-32γ is via a THP-1 cell-produced factor, transferrin, rather than the direct effects of rIL-32γ on epithelial cells. We also characterized a secreted soluble IL-32γ protein in serum of IL-32γ transgenic mouse (TG), but not in that of IL-32α TG. The present results suggest that IL-32γ expression and its genetic variation in individual could be an important aspect of viral infections.
Copyright ? 2012 Elsevier Ltd. All rights reserved.
PMID:
22277801
[PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/22277801