MTB Infection (mtb + infection)

Distribution by Scientific Domains

Selected Abstracts

Tuberculosis in liver transplant recipients: A systematic review and meta-analysis of individual patient data,

Jon-Erik C. Holty
Mycobacterium tuberculosis (MTB) causes substantial morbidity and mortality in liver transplant recipients. We examined the efficacy of isoniazid latent Mycobacterium tuberculosis infection (LTBI) treatment in liver transplant recipients and reviewed systematically all cases of active MTB infection in this population. We found 7 studies that evaluated LTBI treatment and 139 cases of active MTB infection in liver transplant recipients. Isoniazid LTBI treatment was associated with reduced MTB reactivation in transplant patients with latent MTB risk factors (0.0% versus 8.2%, P = 0.02), and isoniazid-related hepatotoxicity occurred in 6% of treated patients, with no reported deaths. The prevalence of active MTB infection in transplant recipients was 1.3%. Nearly half of all recipients with active MTB infection had an identifiable pretransplant MTB risk factor. Among recipients who developed active MTB infection, extrapulmonary involvement was common (67%), including multiorgan disease (27%). The short-term mortality rate was 31%. Surviving patients were more likely to have received 3 or more drugs for MTB induction therapy (P = 0.003) and to have been diagnosed within 1 month of symptom onset (P = 0.01) and were less likely to have multiorgan disease (P = 0.01) or to have experienced episodes of acute transplant rejection (P = 0.02). Compared with the general population, liver transplant recipients have an 18-fold increase in the prevalence of active MTB infection and a 4-fold increase in the case-fatality rate. For high-risk transplant candidates, isoniazid appears safe and is probably effective at reducing MTB reactivation. All liver transplant candidates should receive a tuberculin skin test, and isoniazid LTBI treatment should be given to patients with a positive skin test result or MTB pretransplant risk factors, barring a specific contraindication. Liver Transpl 15:894,906, 2009. 2009 AASLD. [source]

Mycobacterium tuberculosis infection may protect against allergy in a tuberculosis endemic area

C. C. Obihara
Summary Background Epidemiological studies have shown an inverse relation of mycobacterial infection and the frequency of allergic diseases and asthma. Recent evidence suggests that allergic inflammation may be inhibited in the presence of chronic and persistent infections, such as that by Mycobacterium tuberculosis (MTB). The relation of tuberculin skin test (TST) size, an accepted marker of MTB infection and the frequency of allergic disease symptoms has not been reported from an area where MTB infection is endemic. Objective To investigate the association of TST and allergic disease symptoms, in children living in a tuberculosis (TB) endemic area. Methods In this cross-sectional study, 841 children aged 6,14 years from randomly selected household addresses in two poor communities of Cape Town, South Africa, were investigated with TST and standardized International Study on Asthma and Allergies in Childhood-based questionnaire on allergic disease symptoms. Results Children with positive TST (10 mm) were significantly less likely to have allergic disease symptoms, in particular allergic rhinitis (AR) (adjusted odds ratio 0.43; 95% confidence interval 0.24,0.79) than those with negative TST. This association remained significant after adjusting for possible confounders and correcting for the effect of clustering (>1 child per household address) in the sample. There was a significant inverse linear trend in the relation of TST size in millimetre and the frequency of allergic disease symptoms, in particular AR (P<0.001). Conclusions These results of inverse association of strong TST reaction and allergic disease symptoms in children from a TB endemic area are in support of the hypotheses that allergic inflammation may be inhibited by chronic infections, such as MTB. [source]

CD3 expression distinguishes two ,,T cell receptor subsets with different phenotype and effector function in tuberculous pleurisy

N. Yokobori
Summary Tuberculous pleurisy is a naturally occurring site of Mycobacterium tuberculosis (Mtb) infection. Herein, we describe the expression of activation, natural killer (NK) and cell migration markers, as well as effector functions from ,,T cells in peripheral blood (PB) and pleural effusion (PE) from tuberculosis patients (TB). We observed a decreased percentage of circulating ,,T from TB patients and differential expression of NK as well as of chemokine receptors on PB and PE. Two subsets of ,,T cells were differentiated by the CD3/,,T cell receptor (,,TCR) complex. The ,,TCRlow subset had a higher CD3 to TCR ratio and was enriched in V,2+ cells, whereas most V,1+ cells belonged to the ,,TCRhigh subset. In PB from TB, most ,,TCRhigh were CD45RA+CCR7 - and ,,TCRlow were CD45RA+/,CCR7+CXCR3+. In the pleural space the proportion of CD45RA - CCR7+CXCR3+ cells was higher. Neither spontaneous nor Mtb -induced interferon (IFN)-, production was observed in PB-,,T cells from TB; however, PE-,,T cells showed a strong response. Both PB- and PE-,, T cells expressed surface CD107a upon stimulation with Mtb. Notably, PE-,,TCRlow cells were the most potent effector cells. Thus, ,,T cells from PB would acquire a further activated phenotype within the site of Mtb infection and exert full effector functions. As ,,T cells produce IFN-, within the pleural space, they would be expected to play a beneficial role in tuberculous pleurisy by helping to maintain a T helper type 1 profile. [source]

IL-10 down-regulates costimulatory molecules on Mycobacterium tuberculosis -pulsed macrophages and impairs the lytic activity of CD4 and CD8 CTL in tuberculosis patients

SUMMARY Activation of T cells requires both TCR-specific ligation and costimulation through accessory molecules during T cell priming. IFN, is a key cytokine responsible for macrophage activation during Mycobacterium tuberculosis (Mtb) infection while IL-10 is associated with suppression of cell mediated immunity in intracellular infection. In this paper we evaluated the role of IFN, and IL-10 on the function of cytotoxic T cells (CTL) and on the modulation of costimulatory molecules in healthy controls and patients with active tuberculosis (TB). , -irradiated- Mtb (i- Mtb) induced IL-10 production from CD14+ cells from TB patients. Moreover, CD3+ T cells of patients with advanced disease also produced IL-10 after i- Mtb stimulation. In healthy donors, IL-10 decreased the lytic activity of CD4+ and CD8+ T cells whereas it increased ,, -mediated cytotoxicity. Furthermore, we found that the presence of IL-10 induced a loss of the alternative processing pathways of antigen presentation along with a down-regulation of the expression of costimulatory molecule expression on monocytes and macrophages from healthy individuals. Conversely, neutralization of endogenous IL-10 or addition of IFN, to either effector or target cells from TB patients induced a strong lytic activity mediated by CD8+ CTL together with an up-regulation of CD54 and CD86 expression on target cells. Moreover, we observed that macrophages from TB patients could use alternative pathways for i- Mtb presentation. Taken together, our results demonstrate that the presence of IL-10 during Mtb infection might contribute to mycobacteria persistence inside host macrophages through a mechanism that involved inhibition of MHC-restricted cytotoxicity against infected macrophages. [source]