Tuberculosis - Dissertation Example

TB is thus more fatal among children and interferon (IFN)-?-deficient individuals, who still lack granulomatous response (Mustafa et al 449). These are seen in Chest X-ray as lung lesions, and patients also experience muscle wasting (Verreck et al. 8). Pathological characteristics TB patients also have increased C-reactive protein (CRP), while decreased mean corpuscular volume (MCV) and mean corpuscular hemoglobin (MCH) were also observed (Verreck et al. 8). IL-10, transforming growth factor (TGF)-?

, tumor necrosis factor (TNF)-?, and interferon (IFN)-? play various roles in the formation of tuberculous granulomas of TB patients. TNF-? is associated with activation of macrophages. This cytokine, together with IFN-?, enhances the bactericidal activity of monocytes and macrophages, recruitment of these immune cells, and subsequent formation of granulomas (Mustafa et al. 450). IFN-? is produced in response to IL-12 secretion, which is initiated by toll-like receptor (TLR)-2 activation.On the other hand, Il-10 and TGF-?

antagonizes the action of TNF-? and IFN-? respectively, reducing the anti-mycobacterial immune response and allowing the growth of the pathogen within the host cells. In particular, IL-10 induces the macrophages to release soluble TNF-α receptor type 2 (TNFR2), which couples with the cytokine to form an inactive TNF-α-TNFR2 complex. In this regard, a balance among these four is necessary in the optimal immune response against M. tuberculosis. M. tuberculosis is communicated through aerosols and inhaled bacilli.

Upon phagocytosis by alveolar macrophages patrolling the lungs, the bacteria replicate within the host cell. Its survival lies in its ability to block phagosome maturation. Because of the intracellular nature of infection, drugs developed against TB should be able to reach within cells (Feltcher, Sullivan and Braunstein 1582). After which, granuloma forms through the migration of macrophages, lymphocytes and dendritic cells at the infection site. Among these cells, macrophages differentiate into epithelioid cells (EC), or fuse to form multinucleated giant cells (MGC), which is also known as Langhans giant cells.

ECs have better mycobactericidal functions, as seen in their lesser antigen load. On the other hand, the TGF-?- and FasL-expressing MGCs contain more bacterial antigens, and thus allow bacterial growth. In addition, antigen-presenting cells (APCs) with heightened expression of FasL induce apoptosis in T lymphocytes during antigen presentation. Interestingly, ECs that contain mycobacterial antigens may resist apoptosis, and fuse to form MGCs. In contrast, ECs without mycobacteria undergo apoptosis.

These findings show that M. tuberculosis cause inhibition of host cell apoptosis, and the MGCs cause death of antigen-specific T cells. By resisting apoptosis, viral antigens are not presented to immune cells, thus inhibiting recruitment and allowing persistence of the lesion. Persistence of TB infection also partly results from the immune suppression caused by FasL-expressing MGCs (Mustafa et al. 450-454). Thus, despite presenting no clinical symptoms, M. tuberculosis are present in granulomas, and can later reactivate and cause disease (Feltcher, Sullivan and Braunstein 1582).

Diagnosis The gold standard in diagnosing TB remains to be clinical examination, acid-fast bacilli staining of sputum and bacterial culture. Culture of M. tuberculosis