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One third of the earth’s population is infected with Mycobacterium tuberculosis (Mtb), but only 5–10% of the infected individuals develop active tuberculosis (TB) over their lifetime. The remaining 90–95% stay healthy and are called latently infected individuals. They are the biggest reservoir of the tubercle bacilli and identifying the cases of latent TB is a part of the global plan of TB control. From the clinical point of view detection of latent TB infections (LTBI) in individuals with the highest active TB risk including cases of HIV infection, autoimmune inflammatory diseases or cancer, is a priority. This review summarizes the recent findings in the pathogenesis of latent TB, its diagnosis, treatment and prevention.
The polarized response of T helper-2 (Th2) lymphocytes to an allergen is considered to be the main cause of the pathogenesis of asthma. In this study, we asked a question whether M. bovis BCG mycobacteria which are known for the preferential stimulation of T helper-1 (Th1) immunity, diminish the effector functions of Th2 cells from allergic patients upon stimulation with a common house dust mite Der p-1 allergen. Our results allow a positive answer to this question. We demonstrate that BCG modulates the dendritic cell-dependent allergen presentation process and switches naive T lymphocytes towards an anti-allergic Th1 profile.
One third of the earth's population is infected with Mycobacterium tuberculosis, but only 5-10% of the infected individuals will develop active disease over their lifetime. To identify the genes responsible for the variation in the human susceptibility/resistance to tuberculosis (TB) we determined the polymorphisms of three genes crucial for the function of macrophages, in TB patients and healthy controls with no past history of TB. We found no association between the polymorphisms of the NRAMP-INT4, MBL (codons 52, 54, 57) and CD14-159 genes and TB in a Caucasian Polish population. However, we have suggested a possible involvement of CD14 and MBL molecules in the host-mycobacteria interactions on the basis of the significant increase in the serum CD14 and MBL in TB patients compared to healthy controls.
In this study we asked a question whether H. pylori LPS with or without LewisXY (Le) determinants as well as LBP (lipopolysaccharide binding protein) and sCD14 molecules recognizing bacterial LPS may be involved in atherogenesis. Sera from 57 patients with coronary heart disease (CHD), 27 H. pylori infected dyspeptic patients-H.p.(+) and 49 healthy controls (HC) were tested for IgM and IgG to H. pylori LPS expressing LeX (LPS LeX) or LeXY (LPS LeXY) determinants and to a glycine acid extract (GE). Immune complexes (ICs) of Lewis antigens and specific IgM or IgG were also determined. The prevalence of anti-GE IgG and IgA was significantly higher in CHD as compared to HC and the same as in the H.p.(+) group. The highest levels of anti-GE IgG were detected only for CHD group. CHD patients showed upregulation of IgG to LPS LeX and LeXY. In contrast, an upregulation of IgM to such LPSs was found for healthy subjects. The levels of LeY-anti-LeY IgG ICs were higher in CHD patients than in healthy controls similarly to the levels of LBP. There was no difference in sCD14 concentration between CHD and HC groups. The results obtained in this study indicate that H. pylori infections may be the risk factors of atherosclerosis due to: 1) an enhanced humoral response to H. pylori surface antigens, 2) a host predisposition to respond to Lewis determinants present in H. pylori LPS by IgG, 3) increased levels of serum LBP.
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