**4. Conclusion**

Pathogen *M. tuberculosis* by itself as well as particular bacterial lipids are reported to induce loading of macrophages with lipid bodies resulting in formation of foamy macrophages [Russell, 2009]. So it seems that mycobacterial lipids passed by macrophages to each other cause such differentiation of immune cells influencing on total tissue remodelling of the infection site. Inside of such altered foamy macrophages mycobacteria have an access and actually use host lipids from the lipid drops, which leads to their transition into a state similar to the nonreplicating state [Peyron, 2008]. Cultivation of mycobacteria in medium enriched with lipid substances showed that bacilli do form cells with changed morphology and resistant to anti-tuberculosis drugs in such conditions [Nazarova, 2010].

When as a consequence of total 'lipidation' of granuloma macrophages mycobacteria find themselves in the excess of surrounding lipids, this excess induces a dormant state in pathogens. If immune system of the host is active enough, granuloma either undergoes resolution, or remains balanced. But in case of active disease development caseum is accumulated in the centre of some granulomas; this leads to necrosis and collapse of granuloma, and to release of virulent bacilli into airways [Kaplan, 2003]. Since during this release mycobacteria appear to be finally not in stressful conditions and not surrounded or surrounded with a little amount of lipid substances, they might reactivate, as it can be supported by our results where only 0.18-10.6 μМ of oleic acid is required for resuscitation of dormant bacilli.
