Table 2.
Examples of studies on mechanisms underlying the interaction between TB infection and multiple human diseases.
| Disease | Correlation to TB | Relevant findings | References |
|---|---|---|---|
| PULMONARY DISEASE | |||
| Pneumonia | TB infection as a potential etiology | TB infection increases susceptibility to secondary bacterial pneumonia in young children | Oliwa et al., 2015a |
| COPD * | Increases the risk of active TB; TB infection as a potential etiology; | TB infection leads to remodeling of the lung architecture, such as extensive fibrosis, cavitation, traction bronchiectasis, bronchostenosis, or parenchymal lung destruction; the development of bronchiectasis in patients with COPD causes active TB | Dheda et al., 2005; Chakrabarti et al., 2007; Jordan et al., 2010 |
| Lung cancer | TB infection as a potential etiology | TB infection establishes chronic and persistent inflammation; induces production of NO and ROS to bring about DNA damage; develops pulmonary fibrosis | Ardies, 2003; Sharma et al., 2004; Shin et al., 2008 |
| AUTOIMMUNE DISEASE | |||
| Sarcoidosis | TB infection as a potential etiology | M. tuberculosis HSP16 and HSP70 participate in the etiopathogenesis of sarcoidosis; activation of TLRs signaling caused by M. tuberculosis infection involves in the pathogenesis of pulmonary sarcoidosis | Dubaniewicz et al., 2006; Gabrilovich et al., 2013 |
| SLE * | Increases the risk of active TB; TB infection as a potential etiology; | Cross-reactivity between mycobacterial and host self-antigens; antigenic resemblance between mycobacterial glycolipids and host DNA; immune abnormalities and immunosuppressive therapy lead to active TB development | Amital-Teplizki et al., 1989; Yun et al., 2002 |
| METABOLIC DISEASE | |||
| DM * | Increases the risk of active TB; promotes TB progression | Promotes mycobacterial proliferation; enhances CD4+ Th1/Th17 responses and reduces frequencies of Treg cells in active TB patients; reduces Th1/Th17 responses in latent TB patients | Martens et al., 2007; Kumar et al., 2013, 2014 |
| Obesity | Decreases the risk of active TB | The adipose tissue may have immunomodulatory functions against TB infection; the mechanisms are still largely unknown | Wieland et al., 2005; Ordway et al., 2008; Abella et al., 2017 |
| Atherosclerosis | TB infection as a potential etiology | M. tuberculosis HSP65 accelerates the progression of atherosclerosis; both of two diseases accumulates foamy macrophages in the lesion | Peyron et al., 2008; Zhang et al., 2012; Chinetti-Gbaguidi et al., 2015; Wick et al., 2017 |
| Hypovitaminosis D | TB infection as a potential etiology | Vitamin D is essential for production of antimicrobial peptide and promotion of autophagy and phagosomal maturation; the mechanisms of M. tuberculosis-induced hypovitaminosis D is still unclear | Liu et al., 2006; Campbell and Spector, 2012; Azam et al., 2016; Wang J. et al., 2017 |
| CO-INFECTION | |||
| HIV-1 | Increases the risk of active TB; TB infection results in increased viral replication | Depletes M. tuberculosis-reactive T cells; inhibits phagocytosis and autophagy; induces cell death and tissue necrosis | Bell and Noursadeghi, 2017 |
| Helicobacter pylori | Decreases the risk of active TB | Enhances host Th1-type responses with higher level of IFN-γ, IL-2, TNF-α, and CXCL-10 | Perry et al., 2010 |
| Helminth | Commonly occurs in TB patients; disturbs host immune responses to either of infectious pathogens | Reduces M. tuberculosis-antigen specific immune responses; lowers Th1/Th17 responses and elevates Th2 responses | Babu and Nutman, 2016 |
*
COPD, chronic obstructive pulmonary disease; SLE, systemic lupus erythematosus; DM, diabetes mellitus.