The Research On Effect And Mechanisms Of Mast Cell Degranulation On Colonization Of Streptococcus Pneumoniae

Objective: Mast cells(MCs)are currently recognized as effector cells in many settings of the immune response,including host defense,immune regulation,allergy,chronic inflammation,and autoimmune diseases.In different pathogenic microbial infections,mast cells play a useful role in both advantages and disadvantages.Streptococcus pneumoniae is the main pathogens of community-acquired pneumonia.At present,the effect of mast cells on Streptococcus pneumoniae is different,and the specific mechanism is unclear.Therefore,this study is mainly to study the effect of mast cell on Streptococcus pneumoniae infection and the mechanism.Methods: The mast cell activator C48 / 80 was administered by intranasal administration,and the model of mast cell degranulation was established.Mast cell degranulation induced inflammatory reaction in vivo was observed.In vitro culture of mast cells derived from the abdominal cavity,to study its neutrophils and macrophages phagocytic function of phagocytosis.The effect of the corresponding inflammatory factors was verified by IL-6 deficient mice and TNF-? deficient mice.Results: We successfully constructed a mast cell degranulation model and found that mast cell degranulation inhibited the host to remove Streptococcus pneumoniae.Mast cell degranulation could cause increase levels of inflammatory factors and chemokines,increase immune cell raise the airway,ciliated epithelium cell shedding,erythrocyte spill and other inflammatory manifestations.The supernatant of mast cell that treated with C48/80 can inhibit the bactericidal function of macrophage and neutrophil.The load of Streptococcus pneumoniae in the nasopharynx and lung of the IL-6-deficient mice treated with C48 / 80 was significantly lower than wild mice,but the load of Streptococcus pneumoniae in nasopharynx and lung there was no difference between TNF-?-deficient mice and wild mice.Conclusion: Mast cell degranulation could cause strong inflammatory response.Leading to respiratory ciliated columnar epithelial shedding,increased vascular permeability,red blood cell spills,airway inflammation cell recruitment increased,reducing the ability of host to clear Streptococcus pneumoniae.The appropriate inflammatory response was benefited to the host,but the excessive inflammation was damage to the host.Mast cell degranulation inhibited the host to clean Streptococcus pneumoniae and it was related with increased IL-6.