Post-tuberculosis lung disease and inflammatory role players: can we characterise the myriad inflammatory pathways involved to gain a better understanding?

Tuberculosis (TB) remains a global health threat, and even after successful TB treatment, a subset of patients develops serious long-term lung impairments, recently termed post-tuberculosis lung disease (PTLD). Much remains to be discovered, as PTLD as a post-TB disease is a developing field, still in its infancy. The pathogenesis of PTLD is not fully elucidated but has been linked to elevated inflammatory pathways. The complexity of PTLD makes it challenging to pinpoint the specific inflammatory pathways involved in its pathophysiology. Therefore, this paper provides a comprehensive review of inflammatory cytokines and their potential roles in PLTD, with a specific focus on interleukin 6 (IL-6), IL-1, IL-8, tumour necrosis factor-alpha (TNF-alpha), transforming growth factor beta (TGF-beta) and C-Reactive Protein (CRP). We delve into PTLD pathology, discuss its impact on lung function and review risk factors for PTLD. In addition, we summarise the current gaps in knowledge, provide recommendations for measuring inflammatory biomarkers and propose potential directions for future studies. We propose that future studies measure a wide range of inflammatory markers in TB populations with and without PTLD. In addition, studies could isolate peripheral blood mononuclear cells from patient blood to try and identify possible impairments that could be correlated with a PTLD diagnosis. Given that the PTLD field is still in an early stage of development, a comprehensive inflammatory analysis may help to know which pathways are key in PTLD development, and this may ultimately help to predict patients who are at risk. More research is warranted.