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Review
. 2018 Feb 28;27(147):170077.
doi: 10.1183/16000617.0077-2017. Print 2018 Mar 31.

Tuberculosis and lung damage: from epidemiology to pathophysiology

Shruthi Ravimohan  1 , Hardy Kornfeld  2 , Drew Weissman  3 , Gregory P Bisson  3   4
Affiliations
Review

Tuberculosis and lung damage: from epidemiology to pathophysiology

Shruthi Ravimohan et al. Eur Respir Rev. .

Abstract

A past history of pulmonary tuberculosis (TB) is a risk factor for long-term respiratory impairment. Post-TB lung dysfunction often goes unrecognised, despite its relatively high prevalence and its association with reduced quality of life. Importantly, specific host and pathogen factors causing lung impairment remain unclear. Host immune responses probably play a dominant role in lung damage, as excessive inflammation and elevated expression of lung matrix-degrading proteases are common during TB. Variability in host genes that modulate these immune responses may determine the severity of lung impairment, but this hypothesis remains largely untested. In this review, we provide an overview of the epidemiological literature on post-TB lung impairment and link it to data on the pathogenesis of lung injury from the perspective of dysregulated immune responses and immunogenetics.

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Conflict of interest statement

Conflict of interest: Disclosures can be found alongside this article at err.ersjournals.com

Figures

FIGURE 1
FIGURE 1
Mechanisms and radiographic features associated with airflow obstruction and restrictive ventilatory defects in patients with a history of tuberculosis. FEV1: forced expiratory volume in 1 s; FVC: forced vital capacity.
FIGURE 2
FIGURE 2
Immune mediators of tissue remodelling and lung function impairment in tuberculosis. Transcription factors, cytokines and chemokines that drive expression of tissue-degrading enzymes or directly mediate cavitation and/or fibrosis are shown in green. Matrix metalloproteinases (MMP) that promote granuloma and cavitation are depicted in purple. HIF: hypoxia inducible factor; NF: nuclear factor; IL: interleukin; TNF: tumour necrosis factor; TGF: transforming growth factor; IFN: interferon; mtROS: mitochondrial reactive oxygen species. #: IL-1β regulates fibrogenesis in idiopathic pulmonary fibrosis and may play a role in tuberculosis. Pathological processes contributing to the progression of lesions may influence the development of airflow obstruction and restrictive ventilatory patterns of pulmonary impairment.
FIGURE 3
FIGURE 3
Conceptual model of factors that potentially contribute to lung impairment after tuberculosis (TB). MTB: Mycobacterium tuberculosis.
See this image and copyright information in PMC

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