ABSTRACT
AIM: To assess the effectiveness of Lentilactobacillus parafarraginis A6-2 cell lysate for the removal of aluminum (Al), which induces neurotoxicity, and its protective effect at cellular level. METHODS AND RESULTS: The cell lysate of the selected L. parafarraginis A6-2 strain demonstrated superior Al removal compared to live or dead cells. The Al removal efficiency of L. parafarraginis A6-2 cell lysate increased with decreasing pH and increasing temperature, primarily through adsorption onto peptidoglycan. Neurotoxicity mitigation potential of L. parafarraginis A6-2 was evaluated using C6 glioma cells. C6 cells exposed with increasing concentration of Al led to elevated toxicity and inflammation, which were gradually alleviated upon treatment with L. parafarraginis A6-2. Moreover, Al-induced oxidative stress in C6 cells showed a concentration-dependent reduction upon treatment with L. parafarraginis A6-2. CONCLUSIONS: This study demonstrated that L. parafarraginis A6-2 strain, particularly in its lysate form, exhibited enhanced capability for Al removal. Furthermore, it effectively mitigated Al-induced toxicity, inflammation, and oxidative stress.
Subject(s)
Aluminum , Oxidative Stress , Humans , Aluminum/toxicity , Inflammation , Anti-Inflammatory Agents/pharmacologyABSTRACT
Most of the vascular platforms currently being studied are lab-on-a-chip types that mimic capillary networks and are applied for vascular response analysis in vitro. However, these platforms have a limitation in clearly assessing the physiological phenomena of native blood vessels compared to in vivo evaluation. Here, we developed a simply fabricable tissue-engineered vascular microphysiological platform (TEVMP) with a three-dimensional (3D) vascular structure similar to an artery that can be applied for ex vivo and in vivo evaluation. Furthermore, we applied the TEVMP as ex vivo and in vivo screening systems to evaluate the effect of human CD200 (hCD200) overexpression in porcine endothelial cells (PECs) on vascular xenogeneic immune responses. These screening systems, in contrast to 2D in vitro and cellular xenotransplantation in vivo models, clearly demonstrated that hCD200 overexpression effectively suppressed vascular xenograft rejection. The TEVMP has a high potential as a platform to assess various vascular-related responses.
ABSTRACT
Foxp3 stability of vitamin C-treated induced-regulatory T cells (V-iTregs) is superior to that of conventional iTregs (C-iTregs). However, the role of V-iTregs in allograft rejection under vitamin C-deficient conditions, such as those seen in humans, remains unclear. We aimed to elucidate the role of vitamin C treatment on generation and maintenance of iTregs from gulo knockout (Gulo-KO) mice as well as wild type (WT) mice, and in vitro and in vivo suppressive effects of V-iTregs on heart allograft rejection in either Gulo-KO or WT recipient mice. Conversion efficiency of iTregs was similar between C- and V-iTregs in both WT and Gulo-KO mice. V-iTregs from WT or Gulo-KO mice showed better in vitro Foxp3 stability than C-iTregs, although there was no difference between WT V-iTregs and Gulo-KO V-iTregs. Furthermore, V-iTregs from WT or Gulo-KO mice suppressed in vitro T cell proliferation better than C-iTregs. Heterotrophic heart transplantation from BALB/c mice to WT or vitamin C-deficient Gulo-KO C57BL/6J mice was performed following adoptive transfer of C- or V-iTregs. V-iTregs as well as C-iTregs prolonged heart allograft survival in WT and Gulo-KO mice. However, there was no difference between the C- and V-iTreg groups. Supplementation of low- or high-dose vitamin C did not induce significant changes in heart allograft survival in Gulo-KO recipients that had received V-iTregs. In conclusion, V-iTregs do not exert better suppressive effects on heart allograft survival than C-iTregs in either WT or vitamin C-deficient recipients.
