Format

Send to

Choose Destination
J Biol Chem. 2014 Feb 28;289(9):5876-88. doi: 10.1074/jbc.M113.544536. Epub 2014 Jan 7.

Serratia marcescens suppresses host cellular immunity via the production of an adhesion-inhibitory factor against immunosurveillance cells.

Author information

1
From the Laboratory of Microbiology, Graduate School of Pharmaceutical Sciences, University of Tokyo, Tokyo 113-0033, Japan.

Abstract

Injection of a culture supernatant of Serratia marcescens into the bloodstream of the silkworm Bombyx mori increased the number of freely circulating immunosurveillance cells (hemocytes). Using a bioassay with live silkworms, serralysin metalloprotease was purified from the culture supernatant and identified as the factor responsible for this activity. Serralysin inhibited the in vitro attachment of both silkworm hemocytes and murine peritoneal macrophages. Incubation of silkworm hemocytes or murine macrophages with serralysin resulted in degradation of the cellular immune factor BmSPH-1 or calreticulin, respectively. Furthermore, serralysin suppressed in vitro phagocytosis of bacteria by hemocytes and in vivo bacterial clearance in silkworms. Disruption of the ser gene in S. marcescens attenuated its host killing ability in silkworms and mice. These findings suggest that serralysin metalloprotease secreted by S. marcescens suppresses cellular immunity by decreasing the adhesive properties of immunosurveillance cells, thereby contributing to bacterial pathogenesis.

KEYWORDS:

Adhesion; Bacterial Toxins; Cellular Immune Response; Innate Immunity; Insect Immunity; Macrophages; Metalloprotease; Protein Purification; Silkworm

PMID:
24398686
PMCID:
PMC3937657
DOI:
10.1074/jbc.M113.544536
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for HighWire Icon for PubMed Central
Loading ...
Support Center