Cytotoxic response of phagocytes in patients newly infected with pulmonary Mycobacterium tuberculosis determined using plasma tumor necrosis factor-alpha, malondialdehyde, and superoxide dismutase: an observational study

Abstract

Abstract Objective: Pulmonary Mycobacterium tuberculosis infection can trigger cellular and humoral innate immune responses, which may cause death of the pathogen and or host cells/tissue. We aimed to determine the cytotoxic response of phagocytes in patients with pulmonary Mycobacterium tuberculosis infection based on plasma tumor necrosis factor-alpha (TNF-α), malondialdehyde (MDA), and superoxide dismutase (SOD) levels. Methods: In this observational study, patients newly infected with pulmonary Mycobacterium tuberculosis (n = 31; age 37–62 years) and age-matched uninfected volunteers (n = 50) were recruited as test and control volunteers, respectively in Owo, Nigeria. The study protocol was reviewed and approved by the Research and Ethics Committee of the Department of Medical Laboratory Science, Achievers University, Owo, Nigeria (AUO/MLS/VII/2009/212). Anti-hepatitis C virus, human immunodeficiency virus antigen/antibody, hepatitis B virus surface antigen, and plasma TNF-α were determined by enzyme-linked immunosorbent assay, SOD, and MDA were determined by colorimetry, Plasmodium by Giemsa thick blood film staining, and acid-fast bacilli in sputum were detected by Ziehl–Neelsen staining. Results: All participants had normal blood glucose levels and tested negative for human immunodeficiency virus antigen/antibody, anti-hepatitis C virus, hepatitis B virus surface antigen, and Plasmodium spp., and had no medical history of cancer. Infected patients had significantly higher plasma MDA and TNF-α levels and significantly lower SOD levels compared with control subjects (all P < 0.05). Conclusion: Mycobacterium tuberculosis infection elicited a cytotoxic response by phagocytes, evidenced by significant increases in MDA and TNF-α and a significant decrease in SOD levels.