A Spotlight on Liquefaction: Evidence from Clinical Settings and Experimental Models in Tuberculosis

Table 1

The factors involved in liquefaction.

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(A) The upper lobes are privileged sites

 (1) because of their low perfusion/ventilation ratio, which results in:

  (a) an increase in bacillary growth inside individual alveolar macrophages due to the high oxygen pressure in the alveolar space,

  (b) local alkalosis, and thus inhibition of dendritic cell maturation,

  (c) decreased local perfusion, thus delaying the presentation of antigens at the local lymph nodes,

 (2) the mechanical stress of ventilation makes stabilization of a fibrotic lesion more difficult.

(B) The fibrinolytic ability of the macrophages.

(C) Immune response

 (1) as a result of the synchronic effect, which provokes a massive apoptosis/necrosis of infected macrophages in a short period of time,

 (2) induction of high levels of IFN-γ, which promotes fibrinolysis,

 (3) promotion of a massive entry of macrophages into the lesions.

(D) Extracellular bacillary accumulation

 (1) the accumulation of plasminogen and its activation to plasmin induces fibrinolysis and allows the maintenance of the liquefaction

through time,

 (2) generation of a mantle of infected macrophages which maintains the inflammatory response.

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