Project Details


Human campylobacter infections have been increasingly
recognized ass major causes of human illness. Campylobacter
jejuni is now recognized as the most common bacterial cause of
invasive diarrhea in the United States. Campylobacter fetus has
been identified as a cause of bacteremia and disseminated
infection particularly in immunocompromised hosts, such as
patients with AIDS, neonates, and patients with alcoholic liver
disease. Although Campylobacter jejuni is infrequently isolated
from the blood, C. fetus is primarily a bloodstream isolate. The
difference in invasive potential of these two Campylobacter
species may relate to the finding that C. fetus is generally
resistant to the bactericidal effect of human serum while C.
jejuni is serum-sensitive. C. fetus generally have a smooth or
complete lipopolysaccharide (LPS) layer in their outer
membranes. A smooth LPS is known to confer serum-resistance
to other enteric bacterial organisms; however, serum-sensitive
strains of C. fetus also express a complete LPS implying that
other factors contribute to serum-resistance. This proposal
explores the mechanisms of serum-resistance of C. fetus, and the
relationship with high molecular weight surface-array proteins
that migrate at 100k, 125k, or 138k. Preliminary data indicate
that the presence of these surface-array proteins is responsible
for the serum-and phagocytosis-resistance observed because of
failure of C3b to bind to the encapsulated C. fetus strains. We
plan to characterize the biological properties of C. fetus strains
with or without these surface proteins in relation to growth
conditions, complement and phagocytosis-resistance, and
immunological relationships. Subsequently we plan to continue
our chemical and immunological characterization of the proteins
themselves. An important question to be answered is the
mechanism by which these proteins activate C3 but prohibit C3b
from binding to the bacterial cell surface. Using a previously
developed mouse model we will assay the virulence of naturally
and experimentally encapsulated and unencapsulated C. fetus
strains. Using the purified proteins, and monospecific rabbit
antisera and mouse-derived monoclonal antibodies, we will
establish their role in virulence in the mouse model. Then we will
attempt to understand the genetics of production of these
proteins. First we will explore the relationship with plasmids and
then using on of several methods we will clone the genes
responsible for production and expression of these proteins.
Effective start/end date9/1/885/31/06


  • National Institutes of Health: $288,750.00
  • National Institutes of Health: $245,438.00
  • National Institutes of Health: $288,750.00
  • National Institutes of Health
  • National Institutes of Health: $288,750.00
  • National Institutes of Health
  • National Institutes of Health: $281,427.00
  • National Institutes of Health: $210,651.00


  • Medicine(all)
  • Immunology and Microbiology(all)

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