Cytotoxic Response of Phagocytes in Newly Infected Pulmonary Mycobacterium tuberculosis Patients using Plasma TNFα, Malondialdehyde and Superoxide Dismutase

Study Background: Pulmonary Mycobacterium tuberculosis infection can trigger cellular and humoral innate immune response which may cause the pathogen and or the host cell/tissue death. Aims and Objective: This work was designed to determine cytotoxic response of phagocytes in newly infected Pulmonary Mycobacterium tuberculosis patients using plasma TNFα, Malondialdehyde and Superoxide dismutase. Materials and Methods: Newly infected Pulmonary Mycobacterium tuberculosis patients (n=31; age =37 – 62 years) and age matched volunteers who were not infected with Mycobacterium tuberculosis (AFB/Ziehl Neelsen staining negative; n=50) were recruited as test and control volunteers respectively. All subjects investigated in this work have their blood glucose within the reference range; tested negative to HIVAg-Ab; anti-HCV; HBsAg; Giemsa thick blood film for Plasmodium spp.,and have no medical history of malignancy/cancer. Anti-HCV, HIVAg-Ab, HBsAg, plasma TNFα were determined by ELISA; SOD, and MDA by colorimetry, identification of Plasmodium by Giemsa thick blood film staining and identification of Acid Fast Bacilli (AFB). In sputum samples was by Ziehl Neelsen staining. Results: The results obtained in this work showed a significant increase in plasma MDA in Pulmonary Mycobacterium tuberculosis patients compared with the Non-Pulmonary Mycobacterium tuberculosis control subjects(p<0.05).The results obtained also showed a significant decrease in plasma SOD in Pulmonary Mycobacterium tuberculosis patients compared with the Non-Pulmonary Mycobacterium tuberculosis control subjects(p<0.05). There was a significantly higher in plasma TNF-α in Pulmonary Mycobacterium tuberculosis patients compared with the Non-Pulmonary Mycobacterium tuberculosis control subjects(p<0.05).Conclusion: Cytotoxic response of phagocytes has been demonstrated in this work as a feature of Mycobacterium tuberculosis infection which was evidenced by the significant increase in Malondialdehyde (MDA) and TNFα including a significant decrease in Superoxide Dismutase (SOD)