Protection from experimental endotoxemia by a recombinant adeno-associated virus encoding interleukin 10

J Gene Med. 2001 Sep-Oct;3(5):450-7. doi: 10.1002/jgm.213.

Abstract

Background: Interleukin 10 (IL-10) is a homodimeric cytokine that shows considerable clinical promise. Adeno-associated virus (AAV) vectors appear increasingly useful for in vivo gene-transfer applications.

Methods: A recombinant AAV type 2 vector encoding human IL-10 (rAAVhIL10) was constructed by using an adenoviral-free, three-plasmid co-transfection. Cytokine production was measured by using an enzyme-linked immunosorbent assay. Endotoxic shock was induced by lipopolysaccharide (LPS) injection.

Results: As media from rAAVhIL10-infected COS cells caused a dose-dependent blockade of IL-12 secretion from spleen cells of IL-10 knockout (KO) mice challenged with Brucella abortus, it was clear that vector-derived hIL-10 was biologically active in vitro. Intravenous or intramuscular administration of relatively modest levels of rAAVhIL10 (10(10) genomes) to IL-10 KO mice resulted in hIL-10 secretion into the bloodstream, which, at 8 weeks, gave median serum levels of 0.9 and 0.45 pg/ml, respectively. Acute endotoxic shock led to a 33% mortality rate, and severe morbidity, in control IL-10 KO mice, whereas no mortality and little morbidity were seen in IL-10 KO mice given rAAVhIL10 7 weeks earlier.

Conclusions: The findings demonstrate that a modest dose of rAAVhIL10 administered in vivo provides long-term protection against LPS-induced endotoxic shock in a murine model. Thus, this vector may be useful for clinical applications requiring sustained IL-10 expression, for example in the treatment of several autoimmune diseases.

MeSH terms

  • Animals
  • COS Cells / metabolism
  • Dependovirus / genetics*
  • Endotoxemia / chemically induced
  • Endotoxemia / genetics
  • Endotoxemia / prevention & control*
  • Gene Expression
  • Gene Transfer Techniques
  • Genetic Therapy*
  • Genetic Vectors
  • Immunotherapy
  • Interleukin-10 / genetics*
  • Interleukin-10 / metabolism
  • Interleukin-12 / antagonists & inhibitors
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Reverse Transcriptase Polymerase Chain Reaction
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Tumor Necrosis Factor-alpha
  • Interleukin-10
  • Interleukin-12