Type 2 Diabetes Mellitus (T2DM) is a very serious global problem. In Indonesia, this disease attacks at the most productive age; consequently, it can reduce economic status and life expectancy. The pathogenesis of T2DM is very closely related to inflammation and macrophage accumulation. However, no anti-inflammatory agent has been proven to play a role in the management of T2DM. Butyrate is a short chain fatty acid produced from resistant starch fermentation in the intestinal lumen. It is able to bind to GPR41 and GPR43 receptors on monocytes, so that it can change the pattern of cytokine expression, activation, migration and cell differentiation. Hence, it is interesting to examine the anti-inflammation effect of butyrate and the effect on monocyte migration. A total of 37 subjects were examined in this study. They were divided into two groups, with and without butyrate treatment. We analyzed two pro-inflammatory cytokines (Tumor Necrosis Factor TNF-α and Interleukin IL-6) and one anti-inflammatory cytokine, IL 10. Monocytes were isolated in type 1 collagen gel for migration testing using the µ-slide chemotaxis IBIDI. Image analysis used ImageJ and Chemotaxis tool software. There was a significant difference in the TNFα/IL 10 ratio between healthy groups and T2DM. Butyrate also appears to suppress TNFα cytokine production and increase IL10 production. It also decreases the accumulation distance of monocyte migration in T2DM.
1 December 2020 in Journal of Clinical Tuberculosis and Other Mycobacterial Diseases
Tuberculosis infection causes a complex immunological response, where interactions between the pathogen and the host are unique, making it difficult to treat and control this disease. According to WHO, an estimated 1 million children became ill with TB, and 233,000 children died of TB in 2017. Bacillus Calmette-Guérin (BCG) vaccines continue to be the only vaccines to prevent Tuberculosis (TB). Studies suggesting the association of BCG scar with decreased childhood mortality in developing countries have rekindled the interest in BCG scar. However, the direct effect of the BCG scar remains unknown. We examined 76 cases in this study. All Subjects were diagnosed with Tuberculosis. BCG scars were examined directly when physical examination at the BCG vaccination site was performed. Tuberculin Skin Test was performed with 0.1 ml purified protein derivative (PPD) solution (5TU PPD/0.1 ml) injected intradermally. We examined the FOXP3 gene by real-time PCR and the level of Treg byELISA. The comparison of the mean Treg gene expression and the Treg protein content was higher in the positive scar group than in the negative scar group. It shows that Treg plays a role in the Tuberculosis during its active phase development. Treg protein levels were higher in the combination of positive TST and scar. It shows that BCG scarring is an essential marker of a well-functioning immune system. Cheap and straightforward initiatives like early BCG vaccinations, monitoring BCG scarring, and revaccinating scar-negative children could have an enormous immediate impact on global child survival.