Pulmonary Tuberculosis and Lung Cancer – Innate Immunity and the Evolutionary Links of Microbe-induced Inflammation with Cancer: A Case Series

Abstract

Lung cancer is a chronic inflammatory disease. Postprimary tuberculosis (PPTb) is also a manifestation of chronic lung inflammation induced by Mycobacterium tuberculosis. Both acute and chronic inflammation are macrophage-mediated responses. Persistent lung lesions of both PPTb and lung cancer result from chronic nonresolving inflammation. Metabolic adaptation of macrophages through evolutionarily conserved pathways is termed as macrophage polarization. Progressive inflammation induced by microbes activates metabolic alterations in the tissue microenvironment and consequent tumorigenesis by M2-polarized macrophages. The M2 macrophages are poorly bactericidal, permitting intracellular microbial persistence. Both host and microbes undergo metabolic adaptations through hypoxia-inducible factor-induced gene induction. Three cases of PPTb progressing to lung cancer are presented. All cases were initially smear positive for acid-fast bacilli, and progressed to lung cancer while on antituberculosis treatment. Progressive lung inflammation in these cases induced by M. tuberculosis resulted in the progression of infection-induced inflammation to cancer. Smoking and diabetes were risk factors for progression to lung cancer.