Streptococus pneumonia is an important human pathogen, but most are those
installs only transitional nasopharyngeal colonization without causing disease. Use
murine model, this thesis examined the hypothesis that colonization creates purchased
immune responses that protect against subsequent pneumonia. Colonization model of wild-type (WT) and mutant S. pneumonia was set
in outbred mice CD1. Mutants lacking or capsules or lipoproteins, or were
auksotrofy can proliferate in vivo. WT colonization is being protected from subsequent pneumonia
. Mutants were cleared faster than the WT, no immunogenicity and
not protect. When auksotrofy was added, colonization,
immunogenicity and protection have been improved, suggesting the duration of colonization event
is an important factor in determining immunogenicity. This may be a factor
explain poor immunogenicity of other mutants. The mechanism by which previous colonization is being protected from subsequent lethal pneumonia >> << then was determined in a series of studies in inbred CBA / Ca mice. Colonization of the mucosa induced as systemic antibodies to bacterial antigens
surface, but not capsule. There was also evidence of more robust cytokine
production over the next pneumonia, including systemic and mucosal IL-17
responses depending on the presence of CD4-cells. Protection was primarily against
system invasion after pneumonia. Passive transfer experiments and research
using genetically modified mice showed that systemic antibodies was
necessary and sufficient for protection, and in vitro and in natural strattera models have shown that this
opsonophagocytosis through blood and clearance of bacteria. Antigenic protein
purpose of protective serum were determined by Western blot and multiplex bead
ELISA methods. In general, this provision shows that nasal colonization may protect against lethal pneumonia
in mice by opsonophagocytic antibodies against surface proteins so
prevent bacteremia. . << >>