Together with neurons, glial cells form the nervous system; they have nutritive and supportive function also for neurons, isolate the nervous tissues and protect them from foreign bodies in case of injuries.
These cells are known as microglial cells in the Central Nervous System (CNS), and as enteric glial cells in the Enteric Nervous System (ENS); they have identical morphologic and functional features and are functionally and immunologically correlated to the monocyte/macrophage cells.
In Irritable Bowel Syndrome (IBS) and Inflammatory Bowel Disease (IBD), especially in Crohn's disease, a neurodegenerative state is steady. Therefore, changes in the nervous functions could represent an important link between inflammation and neurodegeneration, and this link could be represented by the glial cells, which have demonstrated to control the enteric neuronal functions [1–5]. In particular, alterations of the glial cells may be responsible of the increase of the mucosal barrier permeability, of the neuronal cells' proliferation and of the production of neurokines.
All this confirms the leading role performed by the enteric glia in the inflammation and therefore it could be regarded as an important source of cytokines in the neuroimmune network of the intestine [1–5].
CNS tuberculosis and brain tuberculoma are one of the most serious manifestations of tuberculosis, accounting for 1%-10% of all cases [6, 7]. The infection with MTB leads to an inflammatory tissue destruction . The mechanisms behind this phenomenon are nowadays unknown. The pathogenesis, diagnosis and treatment of CNS-TB have received little attention. A better understanding of its pathogenesis is important to improve existing therapies.
CNS-resident macrophages and microglia are infected with MTB, these cells may be the main cellular target in the CNS [9, 10]. A peculiar characteristic of this bacillus is its ability to infect and multiply inside these cells [6, 9]. Microglial cells reside within the nervous system's parenchyma and in their inactive or resting state have a characteristic "branched" morphology, never seen in resident macrophages of other systems. Microglial cells, in response to a variety of insults such as infection, traumatic injury or ischemia, assume an ameboid shape, and move towards the site of injury [7, 11]. Microglia showing its ameboid phenotype increases its proliferation , motility , fagocytic activity [14, 15] and release of cytokines and reactive oxygen [16–18]. Activated macrophages are key elements in the antimycobacterial immunity: in fact, they secrete specific cytokines against these microorganisms. In particular, the tumor necrosis factor-α (TNF-α) with type 1 cytokines (IFN-γ and IL-1) are essential in the immune response and could be important factor in the immune pathology [6, 19, 20]. Some works have shown that the ingestion of nonopsonized M. tuberculosis by the human microglia is facilitated by the receptor CD14 ; this receptor, together with the integrin β CD-18 and the TNF-α, is involved in the formation of giant mononucleate cells in the swine microglia infected with M. bovis .
Moreover, we decided to study the possible interaction between M. paratuberculosis and the enteroglial cells, in particular the ability to infect glial cells and their consequent activation in antigen-presenting cells, with relevant production of proinflammatory cytokines. Data obtained were correlated to find out analogies and/or differences in the three pathogenic microorganism towards enteric glial and microglial cells.