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Jan 21, 2024
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Mar 8, 2024
Published
Mar 30, 2024
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Abstract

Latent TB infection (LTBI) is a state of persistent immune response to Mycobacterium tuberculosis antigen stimulation but does not yet show clinically active TB. Macrophages can eliminate Mycobacterium tuberculosis through various mechanisms. The aim of this research is to determine the interaction of macrophages against Mycobacterium tuberculosis. Of the 116 articles screened, there were 42 articles that were in accordance with this literature study. Results from the studies reviewed It is possible that some individuals diagnosed with LTBI have recovered from the bacteria, while others have a very small chance of being reinfected.  Granulomas are a pathological sign of Mtb infection. The location of bacteria in the granuloma may influence the immune response necessary to control the infection. Mtb produces lipid and protein effectors that control inflammation and macrophage activity. By preventing Mtb-macrophage interactions and entry into human cells, tuberculosis can be avoided. In addition, many mycobacterial factors play important roles in immune evasion or aid reactivation. The class of proteins encoded by the rpf gene are known as resuscitation promoting factors, which appear to play an important role in reactivation. The Rpf gene is thought to be important in driving mycobacteria out of a dormant (and possibly latent) state.  

Keywords

Latent tuberculosis, macrophages, immune response, Mycobacterium tuberculosis, inflammation, mycrobacteria

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1.
Adiyaksa J, Rukmana A. Latent Tuberculosis: Interaction of Mycobacterium tuberculosis with Macrophages. EKSAKTA [Internet]. 2024Mar.30 [cited 2024Nov.21];25(01):69-80. Available from: https://eksakta.ppj.unp.ac.id/index.php/eksakta/article/view/490

References

  1. W.H.O. (2020). Global Tuberculosis reports: 1997-2022. [Online]. Available: https://www.who.int/.
  2. J. Furin. (2019). Tuberculosis, Lancet, vol. 393, pp. 1642–56.
  3. M. A. Behr, P. H. Edelstein, and L. Ramakrishnan. (2019). Is Mycobacterium tuberculosis infection life long?. BMJ, vol. 367, p. 5770.
  4. CDC. (2021). Centers for Disease Control and Prevention. Latent TB infections in the United States—published estimates.[Online]. Available: https://www.cdc.gov/tb/statistics/ltbi.htm.
  5. A. M. Cadena. (2021). Concurrent infection with Mycobacterium tuberculosis confers robust protection against secondary infection in macaques. PLoS Pathog.14, vol. e1007305.
  6. A. N. Bucsxan et al. (2019). Mechanisms of reactivation of latent tuberculosis infection due to SIV coinfection. J. Clin. Invest, vol. 129, pp. 5254–5260.
  7. F. Hou, K. Xiao, L. Tang, and L. Xie. (2021). Diversity of macrophages in lung homeostasis and diseases. Front. Immunol, vol. 12, p. 753940.
  8. P. S. Hume, S. L. Gibbings, C. V Jakubzick, R. M. Tuder, D. Curran-Everett, and P. M. Henson. (2020). Localization of macrophages in the human lung via design-based stereology. Am. J. Respir. Crit. Care Med, vol. 201, no. 10, pp. 1209–1217.
  9. M. M. Ravesloot-Chávez, E. Dis, and S. A. Stanley. (2021). The innate immune response to mycobacterium tuberculosis infection. Annu. Rev. Immunol, vol. 39, pp. 611–637.
  10. E. Yassine, R. Galiwango, W. Ssengooba, F. Ashaba, M. L. Joloba, and S. Zalwango. (2021). Assessing a transmission network of mycobacterium tuberculosis in an African city using single nucleotide polymorphism threshold analysis. Microbiologyopen, vol. 10, no. 3, p. 1211.
  11. P. Chandra, S. J. Grigsby, and J. A. Philips. (2022). Immune evasion and provocation by mycobacterium tuberculosis. Nat. Rev. Microbiol, p. 1–17.
  12. F. Acosta, P. L. Fernandez, and A. Goodridge. (2021). Do B-1 cells play a role in response to Mycobacterium tuberculosis Beijing lineages?. Virulence, vol. 13, pp. 1–4.
  13. M. M. Berrien-Elliott et al. (2022). Systemic IL-15 promotes allogeneic cell rejection in patients treated with natural killer cell adoptive therapy. Blood. vol. 139.pp. 1177–1183.
  14. N. L. Grant et al. (2022). T cell transcription factor expression evolves over time in granulomas from Mycobacterium tuberculosis-infected cynomolgus macaques. Cell Rep. vol. 39, p. 11082.
  15. Dorhoi, A., Kotze´ , L.A., Berzofsky, J.A., Sui, Y., Gabrilovich, D.I., Garg, A., Hafner, R., Khader, S.A., Schaible, U.E., Kaufmann, S.H.(2020). Therapies for tuberculosis and AIDS: myeloid-derived suppressor cells in focus. J. Clin. Invest, vol. 130, pp. 2789–2799.
  16. C. V Cong, T. T. Ly, and N. M. Duc. (2022). Primary lymphatic tuberculosis in children - Literature overview and case report. Radiol. Case Rep, vol. 17, pp. 1656–1664.
  17. S. K. C. Ganchua, A. G. White, E. C. Klein, and J. L. Flynn. (2020). Lymph nodes-The neglected battlefield in tuberculosis. PLoS Pathog, vol. 16, p. 1008632.
  18. M. Guilliams, G. R. Thierry, J. Bonnardel, and M. Bajenoff. (2020). Establishment and maintenance of the macrophage niche. Immunity, vol. 52, pp. 434–451.
  19. Gideon, H.P., Hughes, T.K., Tzouanas, C.N., Wadsworth, M.H., 2nd, Tu, A.A., Gierahn, T.M., Peters, J.M., Hopkins, F.F., Wei, J.R., Kummerlowe, C. (2022). Multimodal profiling of lung granulomas in macaques reveals cellular correlates of tuberculosis control. Immunity, vol. 55, pp. 827–846 10.
  20. D. Pisu et al. (2021). Single-cell analysis of M. tuberculosis phenotype and macrophage lineages in the infected lung. J. Exp. Med, vol. 218, p. 2021061.
  21. B. B. Ural et al. (2020). Identification of a nerve-associated, lung-resident interstitial macrophage subset with distinct localization and immunoregulatory properties. Sci. Immunol, vol. 5. eaax875.
  22. J. Schyns et al. (2019). Non-classical tissue monocytes and two functionally distinct populations of interstitial macrophages populate the mouse lung. Nat. Commun, vol. 10, p. 39.
  23. L. Huang, E. V Nazarova, S. Tan, Y. Liu, and D. G. Russell. (2020). Growth of Mycobacterium tuberculosis in vivo segregates with host macrophage metabolism and ontogeny. J. Exp. Med, vol. 215, pp. 1135–1152.
  24. T. Laval, L. Chaumont, and C. Demangel. (2021). Not too fat to fight: the emerging role of macrophage fatty acid metabolism in immunity to Mycobacterium tuberculosis. Immunol. Rev, vol. 301, pp. 84–97.
  25. D. Pisu, L. Huang, J. K. Grenier, and D. G. Russell. (2020). Dual RNA-seq of Mtb-infected macrophages in vivo reveals ontologically distinct host-pathogen interactions. Cell Rep, vol. 30, pp. 335–350.
  26. R. Noschka et al. (2021). Gran1: A granulysin-derived peptide with potent activity against intracellular Mycobacterium tuberculosis. Int. J. Mol. Sci, vol. 22.
  27. J. F. Reijneveld et al. (2021). Synthetic mycobacterial diacyl trehaloses reveal differential recognition by human T cell receptors and the C-type lectin Mincle. Sci. Rep, vol. 11, pp. 1–10.
  28. J. Madacki, G. Mas Fiol, and R. Brosch. (2019Update on the virulence factors of the obligate pathogen mycobacterium tuberculosis and related tuberculosis-causing mycobacteria,” Infect. Genet. Evol, vol. 72, pp. 67–77.
  29. J. S. Kim, H. K. Kim, E. Cho, S. J. Mun, S. Jang, and J. Jang. (2022). PE_PGRS38 interaction with HAUSP downregulates antimycobacterial host defense via TRAF6. Front. Immunol, vol. 13, p. 862628.
  30. S. Lata, A. C. Mahatha, S. Mal, U. D. Gupta, M. Kundu, and J. Basu. (2022). Unraveling novel roles of the mycobacterium tuberculosis transcription factor Rv0081 in the regulation of the nucleoid-associated proteins Lsr2 and EspR, cholesterol utilization, and subversion of lysosomal trafficking in macrophages. Mol. Microbiol, vol. 117, no. 5, pp. 1104– 1120.
  31. Y. Fu, J. Shen, Y. Li, F. Liu, B. Ning, and Y. Zheng. (2021). Inhibition of the PERK/TXNIP/NLRP3 axis by baicalin reduces NLRP3 inflammasome-mediated pyroptosis
  32. Y. Feng, M. Li, X. Yangzhong, X. Zhang, A. Zu, and Y. Hou. (2022). Pyroptosis in inflammation-related respiratory disease,” J. Physiol. Biochem, vol. 78, no. 4, pp. 721–737.
  33. et al Ruiz, A., Guzmán-Beltrán, S., Carreto-Binaghi, L. E., Gonzalez, Y., Juá rez, E. (2019). DNA From virulent m. tuberculosis induces TNF-a production and autophagy in M1-polarized macrophages. Microb. Pathog, vol. 132, pp. 166–177.
  34. A. G. Tsolaki, P. M. Varghese, and U. Kishore. (2021). Innate immune pattern recognition receptors of mycobacterium tuberculosis: Nature and consequences for pathogenesis of tuberculosis. Adv. Exp. Med. Biol, vol. 1313, pp. 179–215.
  35. L. Wang, J. Wu, J. Li, H. Yang, T. Tang, and H. Liang. (2020). Host-mediated ubiquitination of a mycobacterial protein suppresses immunity. Nature, vol. 577, no. 7792, pp. 682–688.
  36. P. Ge, Z. Lei, Y. Yu, Z. Lu, L. Qiang, and Q. Chai. (2022). M. tuberculosis PknG manipulates host autophagy flux to promote pathogen intracellular survival. Autophagy, vol. 18, no. 3, pp. 576–594.
  37. H. C. Hawerkamp, L. Geelen, J. Korte, J. Domizio, M. Swidergall, and A. A. Momin. (2020). Interleukin-26 activates macrophages and facilitates the killing of mycobacterium tuberculosis. Sci. Rep, vol. 10, no. 1, p. 17178.
  38. L. A. Ramon-Luing, Y. Olvera, J. Flores-Gonzalez, Y. Palacios, C. Carranza, and Y. Aguilar-Duran. (2022). Diverse cell death mechanisms are simultaneously activated in macrophages infected by virulent mycobacterium tuberculosis. Pathogens, vol. 11, no. 5, p. 492.
  39. Y. Li, Y. Fu, J. Sun, J. Shen, F. Liu, and B. Ning. (2022). Tanshinone IIA alleviates NLRP3 inflammasome-mediated pyroptosis in mycobacterium tuberculosis-(H37Ra-) infected macrophages by inhibiting endoplasmic reticulum stress. J. Ethnopharmacol, vol. 282, p. 114595.
  40. S. Mo, J. Guo, T. Ye, X. Zhang, J. Zeng, and Y. Xu. (2022). Mycobacterium tuberculosis utilizes host histamine receptor H1 to modulate reactive oxygen species production and phagosome maturation via the p38MAPK-NOX2 axis. vol. 13, no. 5. p. 200422.
  41. T. A. P. Siregar, P. Prombutara, P. Kanjanasirirat, N. Kunkaew, A. Tubsuwan, and A. Boonmee. (2022). The autophagy-resistant mycobacterium tuberculosis Beijing strain upregulates KatG to evade starvation-induced autophagic restriction. Pathog. Dis, vol. 80, no. 1, p. 4.
  42. A. Dow, P. Sule, T. J. O’Donnell, A. Burger, J. T. Mattila, and B. Antonio. (2021). Zinc limitation triggers anticipatory adaptations in Mycobacterium tuberculosis. PloS Pathog, vol. 17, no. 5, p. 1009570.