Figure 5
From: The contribution of PARs to inflammation and immunity to fungi
PAR1 promotes inflammation and immunity to Candida through TLR2. WT C57BL6 or tlr2−/− (a) mice (n=8, each group) were infected with C. albicans and treated with PAR1 agonists or antagonists (PAR1-AP and PAR1-ANT) as described in Methods. Periodic acid Schiff staining of sections from stomachs (6 days after the infection) shows the presence of fungal elements (white arrows, inset) and inflammatory cells (black arrows, inset). Bars indicate magnification. One representative of three experiments is shown. (b) The production of oxidant (O2−) and MMP9 was assessed in the lungs or stomach homogenates of infected mice (AU, arbitrary index of scannin densitometry). The bands show the active 92 kDa MMP9. Levels of O2− and MMP9 in uninfected controls were undetectable. (c) Cytokines (pg ml−1) were measured by enzyme-linked immunosorbant assay in culture supernatants (24 h) of dendritic cells isolated from Peyer's patches of uninfected mice and pulsed with live yeasts in vitro for 2 h, before the addition of amphotericin B to prevent fungal overgrowth35 in the presence of 3 × 10−5 M PAR1-AP and PAR1-ANT. Bars are s.e. ifnγ and il10 gene expression was assessed by real-time PCR on CD4+ T cells purified from mesenteric lymph nodes a week after infection.35 *P<0.05, treated vs. untreated. MMP9, matrix metalloproteinase 9; PAR, protease-activated receptor; PMN, polymorphonuclear neutrophil; WT, wild type.
