The Antimycobacterial Celluler Immunity Induced By Immunization With Mycobacterium Tuberculosis H37Ra

Tuberculosis (TB) is a chronic respiratory infectious diseasecaused by Mycobacterium tuberculosis (MTB).Tuberculosis causesapproximately 1.5 billion latent infections,8 million new cases,and2 million deaths annually, making it the most prevalent infectiousdisease in the world[1].The emergence of multidrug-resistanttuberculosis and the pandemic of AIDS have further exacerbatedthe situation[2,3].The host protective immune mechanisms againstinfection with Mycobacterium tuberculosis depend critically onthe interactions and cooperation between monocyte-macrophages,T lymphocytes,and their cytokines,which are sensitive tonutritional insult[4-8]. The only available vaccine against TBBCG,has been extensively evaluated and demonstrated a variableprotective efficacy ranging from 0 to 80% in different field trials. Objectives: To investigate the colonization of H37Ra andBCG in mice , and special antimycobacterial cellular immuneresponse after the immunization with H37Ra or BCG in mice. Methods: 1.BALB/c mice were subcutaneously immunizedwith H37Ra and BCG respectively.Viable MTB were detected inspleens and lungs in BALB/c mice at varier intervals (15days,30days,60days) after immunization, the spleens and lungs of micewere isolated , dissociated and suitable dilutions of thehomogenates were plated on Lowenstein medium.The numbers ofcolony forming unit(CFU) were counted 18 days afterincubation.And the proliferation of T lymphocyte with thestimulus of the purified protein derivative (PPD) was measured byMTT assay, and the expression of interleukin-2(IL-2) and solubleinterleukin-2 receptor (sIL-2R) in the supernatants of culture wasdetermined by ELISA. Results:1.Viable H37Ra and BCG can be located in thespleens and lungs in mice for 60 days at least.2.Compared with SIimmunized by BCG(2.23±0.20 , 2.02±0.38) , the stimulationindex of T lymphocyte proliferation at 30 days and 60 days is 2.81±0.63 and 2.16±0.52 respectively by immunized with H37Ra.These are statistically larger than the unimmunized afterimmunization 30days or 60 days(P<0.05). 3.The expression ofIL-2 in groups immunized with H37Ra or BCG were statisticallylarger than unimmunized after immunization 30days and 60days,and the expression of IL-2 in groups immunized withH37Ra(126.88±8.11pg/ml, 91.26±7.29pg/ml) was statisticallylarger than immunized with BCG(107.15±9.39pg/ml, 77.65±4.23pg/ml) after 30days or 60days (P<0.05).4. The expression ofsIL-2R in groups immunized with H37Ra or BCG werestatistically larger than unimmunized (16.57 ± 1.59 , 15.39 ±2.77)after immunization 30days and 60days, and the expression ofsIL-2R in groups immunized with H37Ra(138.58 ± 7.67pg/ml,127.09±5.47pg/ml) was statistically larger than immunized withBCG(101.94±12.31pg/ml, 93.49±16.38pg/ml) after 30days or60days (P<0.05). Conclusions:H37Ra and BCG can be located and inducespecial antimycobacterial cell immune response in BALB/c mice.And the immunity of H37Ra is slightly better than BCG.