Anti-Macrophage monoclonal antibody

,Scrccl7aronzycvs ccrevisiac as a probiotic has been prescribed for prophylaxis and treatment of gut infected diseases. This study as designed to assess the effects of encapsulated S. ccrevisioc on gastrointestinal tract properties in the animal model. In rats. after X -week feeding by encapsulated and unencapsulated 5. cc revisiae. the mount of the IgA protein ""as determined by ELISA. Rats were euthanized. and the lip er kidney. and intestinal tract were collected for histological analysis. The consumption of S, cerevisiae could increase IgA levels in comparison ith the control group. This increase as significant in the lower parts of the small intestine (p<0.05). In histopathological evaluations: Liver microscopic examination showed fatty change and margination of Kupffer cells as ell as their hyperplasia and hypertrophy. which is a mark for liver regeneration in both groups that received microencapsulated and free probiotic. In spleen structure. in both groups. mild inflammation of the spleen tissue in the form of accumulation of red pulp of er-ythrocytes. hypercellular of this tissue 'vas observed due to hyperplasia oflymphoid follicles and hyperplasia and hepaticophyta of retinal cells and macrophages. The lymphatic structure of the spleen showed relatively intense hyperplasia. In the colon structure. in both groups. hyperplasia of goblet calls along with slight infiltration of inflammaton: cells was noted. Calcium alginate encapsulation considerably improves the yeast viability in simulated gastric juice and simulated intestine juice situations. Also. 5. cerevisiac has positive profits in suitable food absorption and then decreasing diarrhea and other similar gastrointestinal disorders.

Cadmium is a highly toxic metal threatening human and animal health. N-acetyl-L-cysteine (NAC) was reported to play a positive role in disease treatment and immune regulation. The present study aimed to explore the effect of NAC administration on Cd-induced cytotoxicity and abnormal immune response on chicken peritoneal macrophages. Peritoneal macrophages isolated from Isa Brown male chickens were exposed to CdCl2 (20 or 50 mu M) and/or NAC (500 mu M) for different time periods. Results showed that Cd caused dose-dependent damage on chicken peritoneal macrophages characterized by morphologic and ultrastructural alterations, increased cell apoptosis, reactive oxygen species accumulation and mitochondrial injury. Cd exposure inhibited phagocytic activity of chicken peritoneal macrophages, and promoted transcriptional status of pro-inflammatory cytokines (IL-1 beta, IL-6 and TNF-alpha) in both unactivated macrophages and cells in response to lipopolysaccharide (LPS) stimuli. Pretreatment with 500 mu M NAC did not affect growth of normal chicken peritoneal macrophages, while remarkably inhibiting Cd-caused cell death, oxidative stress, and mitochondrial membrane depolarization. NAC pretreatment significantly prevented intracellular Cd2+ accumulation in the Cd-exposed macrophages. Inhibitory effects of NAC on Cd-induced ROS accumulation and mitochondrial injury on chicken macrophages were confirmed in HD-11 macrophage cell line. In addition, NAC pretreatment promoted the phagocytic activity of Cdexposed chicken peritoneal macrophages, and significantly inhibited expression of pro-inflammatory factors (IL-1 beta, IL-6 and TNF-alpha) in both Cd-exposed macrophages and Cd-treated cells in response to LPS stimuli. In conclusion, the present study firstly demonstrated the antagonistic effect of NAC against Cd-caused damage and abnormal immune response on chicken peritoneal macrophages. Protective effect of NAC on chicken macrophages was highly related to its suppression on Cd-induced ROS overproduction, pro-inflammatory reaction and intracellular Cd2+ accumulation.