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,
*
Department of Molecular Biology and Immunology, University of North Texas Health Science Center, Fort Worth, TX 76107;
Departments of Microbiology and Oral Biology, Immunobiology Vaccine Center, University of Alabama, Birmingham, AL 35294; and
Department of Mucosal Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan
The purpose of this study was to determine the nature of the
CD4+ Th cell responses induced after nasal-pulmonary
immunization, especially those coinciding with previously described
pulmonary inflammation associated with the use of the mucosal adjuvant,
cholera toxin (CT). The major T cell population in the lungs of naive
mice was CD4+, and these cells were shown to be
predominantly of Th2 type as in vitro polyclonal stimulation resulted
in IL-4, but not IFN-
, production. After nasal immunization with
influenza Ag alone, Th2 cytokine mRNA (IL-4 and IL-5) levels were
increased, whereas there was no change in Th1 cytokine (IL-2 and
IFN-) mRNA expression. The use of the mucosal adjuvant, CT, markedly
enhanced pulmonary Th2-type responses; however, there was also a Th1
component to the T cell response. Using in vitro Ag stimulation of
pulmonary lymphocytes, influenza virus-specific cytokine production
correlated with the mRNA cytokine results. Furthermore, there was a
large increase in CD4+ Th cell numbers in lungs after nasal
immunization using CT, correlating with the pulmonary inflammatory
infiltrate previously described. Coincidentally, both
macrophage-inflammatory protein-1
(MIP-1) and MIP-1
mRNA
expression increased in the lungs after immunization with Ag plus CT,
while only MIP-1 expression increased when mice were given influenza
Ag alone. Our study suggests a mechanism to foster Th1 cell recruitment
into the lung, which may impact on pulmonary immune responses. Thus,
while Th2 cell responses may be prevalent in modulating mucosal
immunity in the lungs, Th1 cell responses contribute to pulmonary
defenses during instances of intense immune
stimulation.
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