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• W2912498866 abstract "Nothing inspires order more than chaos; thus, medical research has always been preoccupied with the series of epidemics to befall humankind within the modern era. Tuberculosis (TB), however, is an ancient disease, with evidence of this infection seen in the 9000-year-old remains of Neolithic settlement inhabitants.1Hershkovitz I. Donoghue H.D. Minnikin D.E. Besra G.S. Lee O.Y. Gernaey A.M. et al.Detection and molecular characterization of 9000-year-old Mycobacterium tuberculosis from a neolithic settlement in the Eastern Mediterranean.PLoS One. 2008; 3: e3426Crossref PubMed Scopus (262) Google Scholar The relative stability of the Mycobacterium tuberculosis genome over this period is testament to the long-term coexistence of this pathogen and its human host. Indeed, the majority of persons infected will not develop clinical illness from this organism within their lifetime.2Schluger N.W. Rom W.N. The host immune response to tuberculosis.Am J Respir Crit Care Med. 1998; 157: 679-691Crossref PubMed Scopus (360) Google Scholar However, every year, more people die because of tuberculosis than any other infectious disease.3World Health Organization Global tuberculosis report 2017. World Health Organization, Geneva, Switzerland2017Google Scholar This is in spite of the fact that we have had tests to diagnose both active disease and the presence of infection for more than a century, as well as effective first-line drugs for more than half a century. The failure to eliminate TB, and its recent resurgence in a multi–drug-resistant form,4Zumla A. Abubakar I. Raviglione M. Hoelscher M. Ditiu L. McHugh T.D. et al.Drug-resistant tuberculosis--current dilemmas, unanswered questions, challenges, and priority needs.J Infect Dis. 2012; 205: S228-S240Crossref PubMed Scopus (133) Google Scholar reflects, in part, the complex biology of the organism and the disease it causes. Better understanding of the biology of TB, and its implications for TB control, is crucial for progress toward realizing our global commitment to end the TB epidemic by 2030. The latest chapter in this story is published today in the Journal of Allergy and Clinical Immunology: In Practice, in which Yii et al5Yii A. Soh A. Chee C. Wang Y.T. Yuan J.-M. Koh W.-P. Asthma, sinonasal disease, and the risk of active tuberculosis.J Allergy Clin Immunol Pract. 2019; 7: 641-648Abstract Full Text Full Text PDF Scopus (4) Google Scholar investigated the link between asthma, sinonasal disease, chronic bronchitis, and the development of TB. They have implemented a robust study design, a large-scale prospective cohort study, with good participation and follow-up rates, in a setting with a relatively high incidence of TB. This study design has effectively enabled the investigators to overcome the problem of reverse causation, which hampers the interpretation of cross-sectional and case-control studies addressing this question. Yii et al observed a reduced risk of developing active TB in those with asthma and allergic rhinitis–predominant sinonasal disease. This apparent protection was not observed in the chronic bronchitis cohort. The authors hypothesize that this might be due to a TH2-mediated eosinophilic response playing a protective role against mycobacteria in the allergic cohort. However, the evidence for this mechanism remains controversial. TB is known to induce a TH1 response, which suppresses TH2 responses via release of IFN-γ.2Schluger N.W. Rom W.N. The host immune response to tuberculosis.Am J Respir Crit Care Med. 1998; 157: 679-691Crossref PubMed Scopus (360) Google Scholar TH1 cells activate alveolar macrophages, which are involved in phagocytosis and the destruction of mycobacteria.2Schluger N.W. Rom W.N. The host immune response to tuberculosis.Am J Respir Crit Care Med. 1998; 157: 679-691Crossref PubMed Scopus (360) Google Scholar Release of IL-12 from these macrophages creates a positive feedback loop for further TH1 cell recruitment (see Figure 1). TH2 cells are thought to play a negative-feedback role in this pathway, releasing cytokines that inhibit macrophage function in favor of eosinophils, hence their usual suppression.2Schluger N.W. Rom W.N. The host immune response to tuberculosis.Am J Respir Crit Care Med. 1998; 157: 679-691Crossref PubMed Scopus (360) Google Scholar The Mycobacterium bovis-BCG vaccine, which reduces the risk of a TB infection becoming active or severe, promotes TH1 responses and suppresses TH2 responses, highlighting the role of the TH1:TH2 balance in this disease process.6Beasley R. Shirtcliffe P. Harper J.L. Holt S. Le Gros G. Mycobacterium-based vaccines for the prevention of allergic disease: a progress report.Clin Exp Allergy. 2002; 32: 1128-1130Crossref PubMed Scopus (11) Google Scholar Conversely, the phenomenon of eosinophilia in TB has been documented as far back as 1940,7Gill A.M. Eosinophilia in tuberculosis.Br Med J. 1940; 2: 220-221Crossref PubMed Scopus (2) Google Scholar which may indicate that they form part of the host's defense against this bacillus in vivo. In favor of this argument is the in vitro discovery by Driss et al8Driss V. Legrand F. Hermann E. Loiseau S. Guerardel Y. Kremer L. et al.TLR2-dependent eosinophil interactions with mycobacteria: role of alpha-defensins.Blood. 2009; 113: 3235-3244Crossref PubMed Scopus (65) Google Scholar that eosinophils are chemotactic for M bovis, and that they can interact with and destroy these mycobacteria via a Toll-like-receptor-2 mechanism and alpha-defensin release. However, strong TH2 responses have been observed in patients who develop TB despite BCG vaccination and animals that are unable to generate TH2 (and regulatory T) cells have been demonstrated as highly resistant to developing TB infections.9Bhattacharya D. Dwivedi V.P. Maiga M. Van Kaer L. Bishai W.R. Das G. Small molecule-directed immunotherapy against recurrent infection by Mycobacterium tuberculosis.J Biol Chem. 2014; 289: 16508-16515Crossref PubMed Scopus (35) Google Scholar Usually the upregulation of TH2 and suppression of TH1 is associated with active TB, compared with the inverse seen in successfully treated individuals.10Lienhardt C. Azzurri A. Amedei A. Fielding K. Sillah J. Sow O.Y. et al.Active tuberculosis in Africa is associated with reduced Th1 and increased Th2 activity in vivo.Eur J Immunol. 2002; 32: 1605-1613Crossref PubMed Scopus (183) Google Scholar These findings suggest that TH2 cells contribute to the host's susceptibility to M tuberculosis. On balance it appears that if eosinophils do hold antimycobacterial properties in vivo, they contribute too little too late. There are alternative immunological explanations. It has been proposed that the host's antimycobacterial response is not determined by the absolute numbers of TH1 or TH2 cells, but rather by the TH1:TH2 ratio. Perhaps the balance of TH lymphocytes in people with asthma is optimal for defense against mycobacterial infections. Hakonarson et al11Hakonarson H. Maskeri N. Carter C. Grunstein M.M. Regulation of TH1- and TH2-type cytokine expression and action in atopic asthmatic sensitized airway smooth muscle.J Clin Invest. 1999; 103: 1077-1087Crossref PubMed Scopus (124) Google Scholar demonstrated the sequential upregulation in human airway smooth muscle tissue, initially with TH2-type cytokines and receptors and subsequently with TH1-type cytokines and receptors. Zhu et al12Zhu M. Liang Z. Wang T. Chen R. Wang G. Ji Y. Th1/Th2/Th17 cells imbalance in patients with asthma with and without psychological symptoms.Allergy Asthma Proc. 2016; 37: 148-156Crossref PubMed Scopus (50) Google Scholar measured mRNA expression in people with asthma versus controls, and demonstrated significantly increased circulating IFN-γ, and marginally elevated IL-4 without statistical significance, concluding that TH1 and TH2 cells were activated in balance in persons with asthma.12Zhu M. Liang Z. Wang T. Chen R. Wang G. Ji Y. Th1/Th2/Th17 cells imbalance in patients with asthma with and without psychological symptoms.Allergy Asthma Proc. 2016; 37: 148-156Crossref PubMed Scopus (50) Google Scholar The mechanism by which TH1-driven inhibition of TH2 cells is overcome (as described in Figure 1) remains unclear. The balance of the TH1:TH2 immune response may play a role in protection against TB in patients with asthma and rhinitis. Allergy increases the TH2 response and decreases the TH1 response, thus driving the allergic phenotype.6Beasley R. Shirtcliffe P. Harper J.L. Holt S. Le Gros G. Mycobacterium-based vaccines for the prevention of allergic disease: a progress report.Clin Exp Allergy. 2002; 32: 1128-1130Crossref PubMed Scopus (11) Google Scholar It is possible that mycobacteria harness the same property to evade the host's immune system.9Bhattacharya D. Dwivedi V.P. Maiga M. Van Kaer L. Bishai W.R. Das G. Small molecule-directed immunotherapy against recurrent infection by Mycobacterium tuberculosis.J Biol Chem. 2014; 289: 16508-16515Crossref PubMed Scopus (35) Google Scholar Could the harnessing of eosinophils in asthma prevent mycobacteria from being able to use them for its own purposes? To understand the immunological basis of the findings of Yii et al, it would be helpful to know whether there is a difference in TB risk between those with allergic rhinitis (an eosinophil-driven process) and those with chronic rhinosinusitis without nasal polyps (a neutrophil-driven process). Because approximately one-third of the sinonasal cohort may have had a non–allergy- driven disease, the conclusions about the sinonasal disease cohort need to be treated with some caution. It would also have been useful to compare rates of pulmonary to extrapulmonary TB, because the diseases investigated were focused on the respiratory tract. Identification of individuals vaccinated with BCG could be valuable. There is, without doubt, scope for further research within this field. Regardless of the exact mechanism explaining the observations by Yii et al, this work has potential relevance to immunotherapy for TB as discussed in the 2012 review by Guo and Zhao,13Guo S. Zhao J. Immunotherapy for tuberculosis: what’s the better choice?.Front Biosci (Landmark Ed). 2012; 17: 2684-2690Crossref PubMed Scopus (24) Google Scholar which supports the concept of targeting of the TH1/TH2 balance in the treatment of TB. Immunotherapies based on the TH1/TH2 paradigm are emerging for other diseases. They have been shown to be beneficial in cases of unexplained recurrent miscarriage14Liu M. Zhen X. Song H. Chen J. Sun X. Li X. et al.Low-dose lymphocyte immunotherapy rebalances the peripheral blood Th1/Th2/Treg paradigm in patients with unexplained recurrent miscarriage.Reprod Biol Endocrinol. 2017; 15: 95Crossref PubMed Scopus (21) Google Scholar and there are encouraging results being discovered for T-lymphocyte–mediated immunotherapy in people with cancer.15Hoepner S. Loh J.M. Riccadonna C. Derouazi M. Maroun C.Y. Dietrich P.Y. et al.Synergy between CD8 T cells and Th1 or Th2 polarised CD4 T cells for adoptive immunotherapy of brain tumours.PLoS One. 2013; 8: e63933Crossref PubMed Scopus (25) Google Scholar, 16Zanetti M. Tapping CD4 T cells for cancer immunotherapy: the choice of personalized genomics.J Immunol. 2015; 194: 2049-2056Crossref PubMed Scopus (97) Google Scholar Indeed, considering the treatment similarities between TB and cancers, immunotherapies could very well be the next vanguard of TB treatment. Asthma, Sinonasal Disease, and the Risk of Active TuberculosisThe Journal of Allergy and Clinical Immunology: In PracticeVol. 7Issue 2PreviewAlthough asthma is associated with impaired lung immunity, it is unclear whether asthma affects the risk of active tuberculosis (TB). Because the upper and lower airways are immunologically related, sinonasal disease may also modify susceptibility to TB disease. Full-Text PDF" @default.
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