» Articles » PMID: 29491034

Tuberculosis and Lung Damage: from Epidemiology to Pathophysiology

Overview
Journal Eur Respir Rev
Specialty Pulmonary Medicine
Date 2018 Mar 2
PMID 29491034
Citations 189
Authors
Affiliations
Soon will be listed here.
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.

Citing Articles

Nutritional Factors and Food and Nutrition Insecurity in Patients with Tuberculosis.

Mendes Y, Dourado A, de Oliveira P, Rezende A, Sales A, de Sousa G Nutrients. 2025; 17(5).

PMID: 40077748 PMC: 11901461. DOI: 10.3390/nu17050878.


Economic burden of chronic obstructive pulmonary disease and post-tuberculosis sequelae in low- and middle-income countries: a database compiled from a systematic review and meta-analysis.

Lin Y, Walker A, Batta M, Ottilie-Kovelman S, Duchenko A, Brugger C BMJ Public Health. 2025; 2(1):e000441.

PMID: 40018115 PMC: 11816951. DOI: 10.1136/bmjph-2023-000441.


Development of chronic obstructive pulmonary disease after a tuberculosis episode in a large, population-based cohort from Eastern China.

Wang J, Yu L, Yang Z, Shen P, Sun Y, Shui L Int J Epidemiol. 2025; 54(2).

PMID: 39993264 PMC: 11849956. DOI: 10.1093/ije/dyae174.


The prevalence and pattern of post tuberculosis lung disease including pulmonary hypertension from an Australian TB service; a single-centre, retrospective cohort study.

Byrne A, Al-Hindawi Y, Plit M, Yeung L, Rigava S, King M BMC Pulm Med. 2025; 25(1):84.

PMID: 39984904 PMC: 11846343. DOI: 10.1186/s12890-025-03549-5.


A bacterial effector manipulates host lysosomal protease activity-dependent plasticity in cell death modalities to facilitate infection.

Lu Z, Zhang Y, Zhong Y, Qiang L, Ge P, Lei Z Proc Natl Acad Sci U S A. 2025; 122(8):e2406715122.

PMID: 39964716 PMC: 11874418. DOI: 10.1073/pnas.2406715122.


References
1.
Eum S, Kong J, Hong M, Lee Y, Kim J, Hwang S . Neutrophils are the predominant infected phagocytic cells in the airways of patients with active pulmonary TB. Chest. 2009; 137(1):122-8. PMC: 2803122. DOI: 10.1378/chest.09-0903. View

2.
Pasipanodya J, Miller T, Vecino M, Munguia G, Garmon R, Bae S . Pulmonary impairment after tuberculosis. Chest. 2007; 131(6):1817-24. DOI: 10.1378/chest.06-2949. View

3.
Laster S, Wood J, Gooding L . Tumor necrosis factor can induce both apoptic and necrotic forms of cell lysis. J Immunol. 1988; 141(8):2629-34. View

4.
Barlo N, van Moorsel C, Korthagen N, Heron M, Rijkers G, Ruven H . Genetic variability in the IL1RN gene and the balance between interleukin (IL)-1 receptor agonist and IL-1β in idiopathic pulmonary fibrosis. Clin Exp Immunol. 2011; 166(3):346-51. PMC: 3232382. DOI: 10.1111/j.1365-2249.2011.04468.x. View

5.
Long R, Maycher B, Dhar A, Manfreda J, Hershfield E, Anthonisen N . Pulmonary tuberculosis treated with directly observed therapy: serial changes in lung structure and function. Chest. 1998; 113(4):933-43. DOI: 10.1378/chest.113.4.933. View