Pulmonary tuberculosis (PTB) is endemic in many parts of the world.Neutrophils play a crucial role in the effective immune response. There is a growing interest in studying the function of Neutrophils and the complement receptor and their effects on PTB. For the normal function of the neutrophils, β2 integrin (CD18) expressed on leukocytes pairs with α integrin (CD11b) to form membrane attack complex (MAC-1). In a case control study, 40 patients with PTB with a mean age of 31±10.0 years and 78 apparently healthy individuals as controls with a mean age of 28±13.0 years were enrolled to investigate the level and the effect of CD11b+/ CD18+ on neutrophils function, furthermore to investigate the C3b level on the function of neutrophil cells.The neutrophils count in patients (5600±688 cells/µl) was double the count in the controls (2900±574 cells/µl) (p = 0.01). Using Flowcytometry; CD18+/CD11b+ level, mean cell density and count were determined among patients and controls. The results showed significant increase of CD18+/CD11b+ count compared to controls grant median = 2,329, (p = 0.0001), while the level of CD18+/CD11b+ depressed among TB cases compared to controls. Grand median 72.5, (p = 0.01). The decreased level of CD11b+/ CD18+ among TB cases are associated with susceptibility to TB infection three times than controls. Patients showed high levels of C3b compared to controls using ELISA test (p = 0.01); most of the results were above the grant median, 2.4 ng/ml.Interestingly the low level of Mac-1 could be the main reason for over-activation of C3b which was well observed in our study and that agree with previous studies report.The depressed level of MAC-1 affects the affinity of adhesion of complement C3b which decreases the opsnization of MTB bacilli. High neutrophil count among PTB indicates the neutrophil dysfunction due to depressed level of (CD11b+/CD18+ level) or MAC-1 among TB patients. In this study the level of C3b in patients is higher than the controls could point to the failure of activation of C3 to C3a; therefore, the individuals are susceptible to mycobacterial infection because low level of C3a affects the neutrophil function.
Objectives: Seventy five patients with lymphadenopathy who were referred to the Clinic of Lymphadenopathy at the Institute of Endemic Diseases, University of Khartoum were enrolled in our study to detect gene mutation that associated with drug resistance to streptomycin and rifampicin. Materials and methods: Seventy five patients of lymphadenopathy were enrolled for Fine needle aspiration cytology and polymerase chain reaction (PCR). PCR-single strand confirmation polymorphism (PCR-SSCP) for gene mutation was used to detect gene mutation for tuberculous lymphadenitis group. Results: Cytomorphologically, thirty cases showed necrotizing granulomatous tuberculous lymphadenitis (40%) while twenty cases (26%) showed reactive lymph nodes changes. The remaining twenty five cases (34%) had secondary lymph nodes deposits. All cases of tuberculous lymphadenitis group showed similar patterns to H37 Rv with a fragment size of 123 bp when amplified with IS6110 gene primers specific for M. tuberculosis complex, while other groups (reactive and malignant nodes) were negative. For rpsl 43 gene detection, twenty seven cases (27/30) had DNA band patterns identical to H37 while three cases (3/30) were identical to mutant strain that were associated with drug resistance to streptomycin. For the rpoB, all isolates gave identical patterns to H37 Rv strain. Conclusion: PCR is useful to detect Mycobacterium tuberculosis isolates in tuberculous lymphadenitis cases. PCR-SSCP is useful for detection of gene mutation targeting drugs for tuberculosis cases; however, it needs more Supporting tools such as sequencing method to confirm the resistance Tb cases.
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