Radiologic and immunohistochemical correlates of cavitary pulmonary mycobacterial infection: A comparative study of tuberculosis and nontuberculous mycobacteria.

BACKGROUND: Cavitary lung disease caused by Mycobacterium tuberculosis (TB) and nontuberculous mycobacteria (NTM) presents overlapping radiologic features but potentially distinct immunopathologic mechanisms. Macrophage polarization and prothymosin-α (PTMA) expression may contribute to disease progression, but their roles in surgically treated patients remain unclear.

METHODS: We retrospectively analyzed 33 patients who underwent pulmonary resection for TB (n = 17) or NTM (n = 16) infection. Clinical characteristics, CT-based cavity wall thickening scores, and immunohistochemical staining for PTMA, CD68, iNOS, and Arginase-1 were compared. A monocyte migration assay was also performed to evaluate PTMA function.

RESULTS: NTM patients exhibited lower body mass index and fewer comorbidities than TB patients but had a higher relapse rate. Cavity wall thickness correlated with increased PTMA and CD68 expression, particularly in NTM lesions. No significant difference in iNOS or Arginase-1 expression or M1/M2 ratio was observed. M. kansasii was more often linked to severe cavitary disease. PTMA enhanced monocyte migration in a dose-dependent manner in vitro.

CONCLUSION: Radiologic cavity wall thickness may reflect underlying immune dynamics, particularly in NTM. PTMA and CD68 are associated with immune activation and cavity progression in chronic mycobacterial infections. PTMA may serve a dual role as both a histologic marker and a functional regulator of monocyte recruitment. Immunohistochemical analysis revealed no clear M1/M2 polarization shift, suggesting a non-classical or depolarized macrophage phenotype. These findings underscore the potential of PTMA as both a tissue marker and a bioactive mediator in chronic pulmonary infection.