Concerning SIRS injury carries a disproportionately high morbidity and mortality in the elderly to re-search whether Interleukin-6 be risk or protective inflammatory cytokine as different age mice suffered burn and sepsis.Methods We used TBSA burn and burn adding sepsis(S.pneumoniae) mice model to simulate clinic pathological process.IL-6 knock out is used for evaluating the role of Il-6 in this process.we used wild type C56 /BL6 male and IL-6 knock out mice in 2 months and 14 months respectively.In addition to observation of cardiac function,morphology and pathology,we analyzed the IL-6 related cell signal protein: the transcription factor signal transducer and activator of transcription 3 (STAT3) ,the phospho-stat3 (p-stat3) ,the sarco(endo) plasmic reticulum Ca2 + -ATPase 2a (SER-CA2a) ,the suppressor of cytokine signaling 3 (socs3) ,inducible NO synthase (iNOS) .As same time,to isolate car-diomyocytes to measure [Ca2 +]i(intracellular calcium concentrations) .Result Burn complicated by sepsis promoted [Ca2+]i overloading,inflammatory injury and decreased cardiac contractility.Age was a promoter for this procedure.IL-6 deficiency could attenuated this injury process.But the old Il-6 knockout mice didn’t get more benefit like the young,although the aged Il-6 knock out mice lead to milder inflammation in heart pathology.Excepting iNOS,the variations of STAT3,p-stat3,SERCA2a,socs3 was related to cardiac dysfunction,inflammatory injury,and [Ca2 +]i overloading.Conclusions The cytokine Il-6 is a risk factor in burn and sepsis pathogenesis.But IL-6 deficiency seem to be disadvantageous for aged mice suffering from burn and sepsis. Concerning SIRS injury carries a disproportionately high morbidity and mortality in the elderly to re-search whether Interleukin-6 be risk or protective inflammatory cytokine as different age mice suffered burn and sepsis. Methods We used TBSA burn and burn adding sepsis (S. pneumoniae) mice model to simulate clinic pathological process. IL-6 knock out is used for evaluating the role of Il-6 in this process. we used wild type C56 / BL6 male and IL-6 knock out mice in 2 months and 14 months respectively. In addition to observation of cardiac function, morphology and pathology, we analyzed the IL-6 related cell signal protein: the transcription factor signal transducer and activator of transcription 3 (STAT3), the phospho-stat3 (p-stat3), the sarco ( endo) plasmic reticulum Ca2 + -ATPase 2a (SER-CA2a), the suppressor of cytokine signaling 3 (socs3), inducible NO synthase (iNOS) .As same time, to isolate car- diomyocytes to measure [Ca2 +] i calcium concentrations) .Result Burn complicate d by sepsis promoted [Ca2 +] i overloading, inflammatory injury and decreased cardiac contractility. Age was a promoter for this procedure. IL-6 deficiency could attenuated this injury process. But the old Il-6 knockout mice did not get more benefit like the young, although the aged Il-6 knock out mice lead to milder inflammation in heart pathology. Excepting iNOS, the variations of STAT3, p-stat3, SERCA2a, socs3 was related to cardiac dysfunction, inflammatory injury, and [Ca2 +] i overloading. Conclusions The cytokine Il-6 is a risk factor in burn and sepsis pathogenesis. But IL-6 deficiency seem to be disadvantageous for aged mice suffering from burn and sepsis.