Influence of CLL18 on chemoresistance.

<p>Cells were cultured in presence or absence of -TGFbeta or CCL18 in the concentrations indicated for 72 h. After the culture period, medium was changed and the cells were incubated with cisplatin for additional 72 hours at concentrations ranging from 0.4 to 25 µg/ml. Cell survival was measured by MTT assay. The horizontal line indicates the LD₅₀, vertical lines indicate the LD₅₀ for the respective pre-incubation condition (n = 4).</p

Blocking of CD204 abrogates effects mediated by collagen type I monomers.

<p>Preincubation of AM from HD (n=10, Panel A) and IPF patients (n=8, Panel B) with neutralizing antiCD204 (2µg/ml) prior to cell culture abrogated collagen type I monomers induced increase in CCL18 production. Mouse IgG1 served as control. Data are expressed by mean ± SD (*, <i>p</i><0.05).</p

Collagen monomers increase M2 marker production by AM.

<p>M2 cytokine production of BAL cells stimulated with monomers of various collagen types. M2 cytokine production of BAL cells from 5 additional patients with IPF are depicted in black and 5 additional experiments with BAL cells from healthy donors are depicted in grey. <b>Panel A</b> shows CCL18 production following stimulation with rat collagen-I (Col 1R; 100µg/ml), human collagen-I (Col I, 100 µg/ml), human collagen-III (Col III, 100 µg/ml), human collagen-IV (Col IV, 100 µg/ml), human collagen-V (Col V, 100 µg/ml). <b>Panel B</b> shows IL-1ra production following the same stimulation protocol. <b>Panel C</b> shows CCL2 production. *p<0.05.</p

Estimated effects from univariate Cox regression models for acute exacerbations.

<p><b>Definition of abbreviations:</b> FVC: forced vital capacity; n.s.: not significant.</p><p>Estimated effects from univariate Cox regression models for acute exacerbations.</p

Mean CCL18 levels of all T stages was significantly increased compared with controls (p<0.0002).

<p>In addition, there was a significant difference between patient groups with lowest versus the two highest T-stages.</p

Surfactant proteins in absence or presence of indomethacin alone or in combination with PGE2.

<p>A) AECII were cultured without or with the cyclooxygenase inhibitor indomethacin (1 µM) and SP-A1, SP-A2; SP-B; SP-C and SP-D mRNA were measured by real-time PCR after culture. Relative Expression of surfactant proteins in cultures without indomethacin (C, hatched bar) were used to calculate the percentage of remaining surfactant expression after cyclooxygenase inhibition (indomethacin, n = 5)). B) Change of relative expression of surfactant proteins in cultures without (C; left panel) and with inhibition of cyclooxygenase by indomethacin (1 µM) and substitution with external PGE2 (10 nM, right panel) measured by real-time PCR. Bar charts show mean ± SD (surfactant proteins n = 8; rE = relative expression; c = control; PGE2 = prostaglandin E2).</p

Spontaneous macrophage derived chemokine production in IPF patients w/o acute exacerbation.

<p>Boxplots of the spontaneous production of A: CCL2, B: CCL17, C: CCL18, D: CCL22, E: IL-1ra, F: TNF-α, G: IL-1β, H: IL-8 and I: CXCL1 protein by BAL cells of patients with IPF. The dark grey boxplots represent patients who suffered from an acute exacerbation (AE, n = 12), the light grey represent patients who did’t suffer from an AE at timepoint of BAL (NoAE, n = 59) (* p<0.05, ** p<0.01, n.s. = not significant).</p