lowing both bleomycin injury and bleomycin injury with day 0 murine AFSC treatment. Other cytokine modulations in BAL and lung tissue were detected, but were found not to be statistically significant. Furthermore, the cellular component of BAL fluid, which was comprised mainly of macrophages, lymphocytes and neutrophils was analyzed to determine the effect of cytokine modulation on inflammatory cell populations. Inflammatory cell recruitment to the lung, a key characteristic of the fibrotic and bleomycin injured lung, decreased overall following bleomycin injury, and increased moderately following murine AFSC treatment. When individual cell populations were examined, cell populations, which express CCR2 and are 8913470 thus responsive to CCL2 such as macrophages and lymphocytes increased after bleomycin injury and decreased following murine AFSC treatment. Finally, neutrophils rose following murine AFSC treatment, which is consistent with complement activation C5a observed in murine AFSC BCTC web treated cohorts. CCL2 concentrations in BAL from animals 3 days postbleomycin injury were further quantified via ELISA. BAL collected from control mice exhibited CCL2 levels of 42.6764.01 pg/lung, while CCL2 levels in BAL from bleomycin-injured animals increased 2-fold to 84.97613.87 pg/lung. Animals that received murine AFSC at day 
0 demonstrated a decrease in CCL2 levels to 42.7865.10 pg/lung . BAL collected from bleomycin-injured animals 28 days post-injury demonstrated an increase in CCL2 when compared to control animals, in contrast with animals that received murine AFSC at either day 0 or day 14, which showed significantly decreased levels of CCL2 at the 28 day post-injury time point and 32.4865.49 pg/lung, respectively). AFSC Treatment Inhibits Loss of Pulmonary Function Associated with the Development of Pulmonary Fibrosis 28 Days Post-bleomycin Injury In vivo AFSC Treatment Inhibits Pulmonary Fibrosis CCL2 has been previously shown to promote collagen synthesis in fibroblasts though induction of the TGF-b pathway. To determine what if any impact increased CCL2 concentrations found in BAL post-bleomycin injury could have on collagen synthesis by fibroblasts, 3T3 fibroblasts were exposed to increasing concentrations of recombinant CCL2 in culture. This resulted in a 2.5-fold increase in collagen synthesis when cells were exposed to 100 pg/ml CCL2, similar to CCL2 levels detected in bleomycininjured murine BAL. BAL samples analyzed via ELISA in 6 AFSC Treatment Inhibits Pulmonary Fibrosis . BAL from animals 28 days post-bleomycin injury induced a significant increase in collagen synthesis when compared to control animals. Treatment of bleomycininjured mice with AFSC at days 0 or 14 post-injury resulted in production of BAL that induced significantly less collagen synthesis when compared to BAL from bleomycin-injured mice, with 3.34-fold and 1.77-fold reductions in 3T3 collagen synthesis respectively. Increases in cell number following exposure to CCL2 or BAL samples were not statistically significant at the conclusion of the assay, thus indicating that increases in collagen measured 7906496 were 7 AFSC Treatment Inhibits Pulmonary Fibrosis due to increased collagen synthesis and not increases in cell number. These data demonstrate that AFSC are immunomodulatory in the bleomycin lung injury model, and that AFSC have the capacity to modulate key pro-inflammatory/pro-fibrotic cytokines, most notably CCL2. The link to CCL2 mediated processes following bleomycin injur
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