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. Author manuscript; available in PMC: 2012 May 7.
Published in final edited form as: J Theor Biol. 2011 Feb 3;276(1):199–208. doi: 10.1016/j.jtbi.2011.01.054

Figure 1.

Figure 1

Diagram of interactions between various cell types and anthrax toxin considered in the model equations, given by Eqs. 16 in the text. Spores (S) enter the airway and are readily phagocytosed by resident alveolar phagocytes (A) which become host cells (H). After phagocytosis, the host cells (H) migrate to the Thoracic/Mediastinal Lymph Nodes (TMLN) compartment. The intracellular spores (Si) germinate en route to the TMLN into vegetative intracellular bacteria (Bi) which can replicate before destroying their host cell via the production of toxins. (Si, Bi, and intracellular toxins are not modeled explicitly.) After destroying the host cell, the bacteria are released and become extracellular bacteria (Be) which grow and produce anthrax toxins (TA). Resident cells (E) as well as soluble components of the innate immune system in the TMLN are the first to encounter the anthrax bacteria and attempt to kill some of the bacteria; however, anthrax induces lysis of these cells after their interaction, keeping killing of bacteria by these resident cells to a minimum. Signals elicited upon death of these cells, attract neutrophils (N) from the blood stream into the TMLN. Neutrophils are partially effective against the bacteria, although the anthrax toxins inhibit neutrophil priming, mobility, and phagocytosis.