Rationale:　Asthma-induced　inflammation　has　been　shown　to　increase　the　risk　of　deep　vein　thrombosis　(DVT),　but　the　underlying　mechanisms　remain　unclear.　Objective:　To　verify　the　associations　between　asthma　exacerbation　and　the　occurrence　and　development　of　DVT　and　explore　the　potential　pathophysiological　mechanisms　at　the　molecular　level.　Methods　and　results:　By　coculturing　activated　and　unactivated　mast　cells　with　endothelial　cells,　we　found　that　activated　mast　cells　could　lead　to　an　increase　in　inflammatory　factors.　In　contrast,　this　effect　was　significantly　attenuated　when　we　cocultured　toll-like　receptor　4　(TLR4)-knockdown　mast　cells　with　endothelial　cells.　In　a　mouse　model　of　DVT　induced　by　partial　ligation　of　the　inferior　vena　cava,　we　demonstrated　that　asthma　exacerbates　DVT　in　mice.　DVT　was　significantly　attenuated　in　vivo　after　the　administration　of　mast　cell　degranulation　and　TLR4　inhibitors　to　asthmatic　mice,　whereas　the　infusion　of　differentiated　MCs　into　mice　exacerbated　thrombosis.　However,　thrombosis　was　not　significantly　aggravated　after　the　infusion　of　TLR4-knockdown　mast　cells.　Inhibition　of　MC　degranulation　as　well　as　TLR4　receptor　expression　attenuated　local　and　systemic　inflammation　in　asthmatic　mice,　and　reinfusion　of　NC-MCs　reversed　this　effect,　whereas　the　reversal　and　degranulation　of　MCs　were　attenuated　after　reinfusion　of　TLR4-knockdown　MCs.　The　infusion　of　differentiated　MCs　into　asthmatic　mice　with　inhibited　MC　degranulation　and　systemic　TLR4　resulted　in　significant　increases　in　AKT,　P38,　JNK,　and　ERK,　whereas　the　infusion　of　TLR4-knockdown　MCs　resulted　in　significantly　reduced　increases　in　AKT,　P38,　JNK,　and　ERK.　Conclusions:　Asthma　may　exacerbate　DVT　via　mechanisms　related　to　mast　cells,　which　may　exacerbate　DVT　through　endothelium　inflammation　and　the　upregulation　of　AKT,　P38,　JNK,　etc.,　which　is　mediated,　at　least　in　part,　by　TLR4.