Mathematical modeling of tuberculosis bacillary counts and cellular populations in the organs of infected mice.
<h4>Background</h4>Mycobacterium tuberculosis is a particularly aggressive microorganism and the host's defense is based on the induction of cellular immunity, in which the creation of a granulomatous structure has an important role.<h4>Methodology</h4>We present here a...
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oai:doaj.org-article:e6d1ef2ed90545a084ff5719e4cc30822021-11-18T06:34:51ZMathematical modeling of tuberculosis bacillary counts and cellular populations in the organs of infected mice.1932-620310.1371/journal.pone.0012985https://doaj.org/article/e6d1ef2ed90545a084ff5719e4cc30822010-09-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/20886087/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Mycobacterium tuberculosis is a particularly aggressive microorganism and the host's defense is based on the induction of cellular immunity, in which the creation of a granulomatous structure has an important role.<h4>Methodology</h4>We present here a new 2D cellular automata model based on the concept of a multifunctional process that includes key factors such as the chemokine attraction of the cells; the role of innate immunity triggered by natural killers; the presence of neutrophils; apoptosis and necrosis of infected macrophages; the removal of dead cells by macrophages, which induces the production of foamy macrophages (FMs); the life cycle of the bacilli as a determinant for the evolution of infected macrophages; and the immune response.<h4>Results</h4>The results obtained after the inclusion of two degrees of tolerance to the inflammatory response triggered by the infection shows that the model can cover a wide spectrum, ranging from highly-tolerant (i.e. mice) to poorly-tolerant hosts (i.e. mini-pigs or humans).<h4>Conclusions</h4>This model suggest that stopping bacillary growth at the onset of the infection might be difficult and the important role played by FMs in bacillary drainage in poorly-tolerant hosts together with apoptosis and innate lymphocytes. It also shows the poor ability of the cellular immunity to control the infection, provides a clear protective character to the granuloma, due its ability to attract a sufficient number of cells, and explains why an already infected host can be constantly reinfected.Antonio BruPere-Joan CardonaPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 5, Iss 9, p e12985 (2010) |
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Medicine R Science Q Antonio Bru Pere-Joan Cardona Mathematical modeling of tuberculosis bacillary counts and cellular populations in the organs of infected mice. |
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<h4>Background</h4>Mycobacterium tuberculosis is a particularly aggressive microorganism and the host's defense is based on the induction of cellular immunity, in which the creation of a granulomatous structure has an important role.<h4>Methodology</h4>We present here a new 2D cellular automata model based on the concept of a multifunctional process that includes key factors such as the chemokine attraction of the cells; the role of innate immunity triggered by natural killers; the presence of neutrophils; apoptosis and necrosis of infected macrophages; the removal of dead cells by macrophages, which induces the production of foamy macrophages (FMs); the life cycle of the bacilli as a determinant for the evolution of infected macrophages; and the immune response.<h4>Results</h4>The results obtained after the inclusion of two degrees of tolerance to the inflammatory response triggered by the infection shows that the model can cover a wide spectrum, ranging from highly-tolerant (i.e. mice) to poorly-tolerant hosts (i.e. mini-pigs or humans).<h4>Conclusions</h4>This model suggest that stopping bacillary growth at the onset of the infection might be difficult and the important role played by FMs in bacillary drainage in poorly-tolerant hosts together with apoptosis and innate lymphocytes. It also shows the poor ability of the cellular immunity to control the infection, provides a clear protective character to the granuloma, due its ability to attract a sufficient number of cells, and explains why an already infected host can be constantly reinfected. |
format |
article |
author |
Antonio Bru Pere-Joan Cardona |
author_facet |
Antonio Bru Pere-Joan Cardona |
author_sort |
Antonio Bru |
title |
Mathematical modeling of tuberculosis bacillary counts and cellular populations in the organs of infected mice. |
title_short |
Mathematical modeling of tuberculosis bacillary counts and cellular populations in the organs of infected mice. |
title_full |
Mathematical modeling of tuberculosis bacillary counts and cellular populations in the organs of infected mice. |
title_fullStr |
Mathematical modeling of tuberculosis bacillary counts and cellular populations in the organs of infected mice. |
title_full_unstemmed |
Mathematical modeling of tuberculosis bacillary counts and cellular populations in the organs of infected mice. |
title_sort |
mathematical modeling of tuberculosis bacillary counts and cellular populations in the organs of infected mice. |
publisher |
Public Library of Science (PLoS) |
publishDate |
2010 |
url |
https://doaj.org/article/e6d1ef2ed90545a084ff5719e4cc3082 |
work_keys_str_mv |
AT antoniobru mathematicalmodelingoftuberculosisbacillarycountsandcellularpopulationsintheorgansofinfectedmice AT perejoancardona mathematicalmodelingoftuberculosisbacillarycountsandcellularpopulationsintheorgansofinfectedmice |
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