Antigen stimulation of TH2 cells augments acute bacterial sinusitis in mice.
BACKGROUND
Previously, we showed that an ongoing nasal allergic response augmented bacterial sinusitis in mice. In those experiments mice were sensitized to ovalbumin (OVA) by means of intraperitoneal injections of OVA-alum and then exposed to OVA intranasally before being infected with Streptococcus pneumoniae.


OBJECTIVE
We sought to study the importance of TH2 cells and to eliminate potential alum effects.


METHODS
In this study we sensitized mice by adoptively transferring OVA-specific TH2- or TH1-skewed cells.


RESULTS
TH2 passive sensitization followed by intranasal OVA showed a robust local eosinophilic response (5-fold increase) compared with that seen in mice with only TH2 passive sensitization alone (P <.001). Mice with TH2 passive sensitization and intranasal OVA exposure followed by infection showed an increase in the number of recovered S pneumoniae (P <.05) and an increase in sinus inflammation compared with that seen in those with infection alone (P <.01). In contrast, mice passively sensitized with TH1 followed by intranasal OVA exposure and infection showed no significant increase in the recovery of S pneumoniae and sinus inflammation compared with those with infection alone.


CONCLUSIONS
These data support the importance of antigen-stimulated TH2 cells in the augmented response to infection in allergic mice. Whether the increased infection is related to the direct effect of TH2 cells and their cytokines or subsequent recruitment of other cells, such as eosinophils, will be determined in further studies.
Yu
Xiaohong
X
Department of Surgery, Section of Otolaryngology--Head and Neck Surgery, University of Chicago, IL 60637, USA.
Sperling
Anne
A
Blair
Christopher
C
Thompson
Kenneth
K
Naclerio
Robert
R
D000208:Acute Disease; D019264:Adoptive Transfer; D000818:Animals; D001424:Bacterial Infections / Q000209:etiology*; D051379:Mice; D008807:Mice, Inbred BALB C; D010047:Ovalbumin / Q000276:immunology*; D012852:Sinusitis / Q000209:etiology*; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology / Q000502:physiology*
D010047:Ovalbumin