Background:Inflammation is often linked with the progress and poor outcome of lung cancer.The understanding of the relationship between tumor-associated macrophages(TAMs) and lung cancer cells involves in the underlying mechanism of inflammatory cytokine production.Toll-like receptors(TLRs) are engaged in promoting the production of pro-inflammatory cytokines and play an important role in tumor immunology.Methods:To investigate the mechanisms by which TAMs influence the production of pro-inflammatory cytokines in lung cancer cells,we established an in vitro coculture system using TAMs and human nonsmall cell lung cancer(NSCLC) cell line SPC-A1.Levels of interleukin(IL)-1β,IL-6 and IL-8 in SPC-A1 were evaluated by RT-PCR and cytometric bead array assay after being cocultured with TAMs.Expression changes of TLRs and TLRs signaling pathway proteins in SPC-A1 were further confirmed by RT-PCR and western blot.The level changes of IL-1β,IL-6 and IL-8 in SPC-A1 were also detected after the stimulation of TLRs agonists.Results:We found that the phenotype markers of TAMs were highly expressed after stimulating human monocyte cell line THP-1 by phorbol-12-myristate-13-acetate(PMA).Higher mRNA and supernate secretion levels of IL-1β,IL-6 and IL-8 were detected in SPC-A1 after being cocultured with TAMs.We also found that TLR1,TLR6 and TLR7 were up-regulated in SPC-A1 in the coculture system with TAMs.Meanwhile,TLRs signaling pathway proteins were also significantly activated.Moreover,pre-treatment with agonist ligands for TLR1,TLR6 and TLR7 could dramatically promote inductions of IL-1β,IL-6 and IL-8.Conclusions:These findings demonstrated that TAMs may enhance IL-1β,IL-6 and IL-8 expressions via TLRs signaling pathway.We conclude that TAMs contribute to maintain the inflammation microenvironment and ultimately promote the development and progression of lung cancer. Background: Inflammation is often linked with the progress and poor outcome of lung cancer. The understanding of the relationship between tumor-associated macrophages (TAMs) and lung cancer cells involves in the underlying mechanism of inflammatory cytokine production. Like-like receptors (TLRs) are engaged in promoting the production of pro-inflammatory cytokines and play an important role in tumor immunology. Methods: To investigate the mechanisms by which TAMs influence the production of pro-inflammatory cytokines in lung cancer cells, we established an in vitro coculture system using T cells and human nonsmall cell lung cancer (NSCLC) cell line SPC-A1. Levels of interleukin (IL) -1β, IL-6 and IL-8 in SPC-A1 were evaluated by RT-PCR and cytometric bead array assay after being cocultured with TAMs.Expression changes of TLRs and TLRs signaling pathway proteins in SPC-A1 were further confirmed by RT-PCR and western blot. level levels of IL-1β, IL-6 and IL-8 were also detected after the stimulation of TLRs agonists. Results: We found that the phenotype markers of TAMs were highly expressed after stimulating human monocyte cell line THP-1 by phorbol-12-myristate- 13-acetate (PMA) .Higher mRNA and supernate secretion levels of IL- 1β, IL-6 and IL-8 were detected in SPC-A1 after being cocultured with TAMs. We also found that TLR1, TLR6 and TLR7 were up-regulated in SPC-A1 in the coculture system with TAMs. Proteins were also significantly activated.Moreover, pre-treatment with agonist ligands for TLR1, TLR6 and TLR7 could dramatically promote inductions of IL-1β, IL-6 and IL-8.Conclusions: Twenty- IL-6 and IL-8 expressions via TLRs signaling pathway. We conclude that TAMs contribute to maintain the inflammation microenvironment and ultimately promote the development and progression of lung cancer.