Colonization model of wild-type (wt) and mutant p.

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. . << >>