Mouse Anti-M. tuberculosis 38kDa Monoclonal antibody, clone ITM83

Tuberculosis is highly contagious disease that can be transmitted between humans and animals. Asian elephants (Elephas maximus) in captivity live in close contact with humans in many Asian countries. In this study, we developed an interferon gamma release assay (IGRA) for elephant TB detection using antigens from the MTB complex (MTBC) and nontuberculous mycobacteria (NTM) as stimulating antigens (PPD, ESAT6, CFP10) to elicit a cell-mediated immune response (CMIR). The developed assay was applied to an elephant herd of more than 60 animals in Thailand, and the results were compared with those obtained through serological detection. IGRA has sufficient sensitivity for detecting elephant interferon gamma (eIFN gamma) from specific antigen-stimulated PBMCs. Among 60 animals tested, 20 samples (33.3%) showed negative results for both MTBC and NTM infection. Eighteen samples (30%) showed positive responses against PPD from M. bovis and/or ESAT6 and CFP10, indicating MTBC infection. In contrast, only 15.6% showed seropositivity in a commercial serological test kit for elephant TB. The discrepancies between serological and CMIR highlight that the two methods may detect different stages of elephant TB. Therefore, employing both tests may enable them to complement each other in correctly identifying elephants that have been exposed to MTBC.

Background: Mycobacterium vaccae nebulization imparted protective effect against allergic asthma in a mouse model. The TGF-beta/Smad signal transduction pathway plays an important role in allergic bronchial asthma. However, the effect of M. vaccae nebulization on the TGF-beta/Smad signal transduction pathway in mouse models of allergic asthma remains unclear. This study investigated the preventive effect of M. vaccae nebulization during bronchial asthma in a mouse model and elucidate the implication of TG beta/Smad signal transduction pathway in the process. Methods: In total, 24 female Balb/c mice were randomized to normal control (group A), asthma control (group B), and M. vaccae nebulization (group C) groups. Both groups B and C were sensitized using ovalbumin for establishment of the asthmatic model; group A received phosphate-buffered solution. Prior to the establishment of asthma, Group C was nebulized with M. vaccae. Airway responsiveness was measured in all the groups, using a noninvasive lung function machine before and 24 h after establishment of the asthmatic model. The animals were then harvested, and bronchoalveolar lavage fluid (BALF) and lung tissue were collected. The total cell counts in BALF was estimated. Protein expression ofTGF-beta 1,T beta R1,Smad1, and Smad7 was detected by immunohistochemistry. The population of CD3(+)gamma delta T, IL-13(+)CD3(+)T,TGF-beta(+)CD3(+)T, IL-13(+)CD3(+)gamma delta T, and TGF-beta(+) CD3(+)gamma delta T cells were detected by flow cytometry. One-way analysis of variance for within-group comparisons, the least significant difference t-test or Student-Newman-Keuls test for intergroup comparisons, and the nonparametric rank sum test for analysis of airway inflammation scores were used in the study. Results: The eosinophil count; protein expression ofTGF-beta 1,T beta R1, and Smad1; and percentages of CD3(+)gamma delta T and IL-13(+)CD3(+)T cells were significantly lower in the M. vaccae nebulization group than in the asthma control group (P < 0.01). There were significant intergroup differences in the percentages ofTGF-beta(+)CD3(+)T and IL-13(+)CD3(+)gamma delta T cells (P < 0.05). Conclusions: Mycobacterium vaccae nebulization could confer protection against allergic bronchial asthma by reducing airway responsiveness and alleviating airway inflammation in mice. The underlying mechanism might be attributed its effect on the deregulated expression of TGF-beta 1,T beta R1,Smad1, and Smad7 of the TGF-beta/Smad signal transduction pathway.