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.