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Curdlan, a β-1,3/1,6-glucan found in Alcaligenes faecalis (A. faecalis) wall, activates innate and humoral immunity. The aim of this study is to evaluate whether pretreated rats with A. faecalis A12C could prevent sepsis disturbances and identify the immunomodulatory mechanisms involved. Experiments occurred in two stages: a survival study with 16 rats randomly divided into septic (SC) (n = 8) and septic pretreated (SA) (n = 8) groups and 45 rats divided into four groups: healthy (AGUSAN) (n = 9), septic (AGUIC) (n = 13), septic pretreated (AGUIA) (n = 14), and healthy pretreated (AGUSTO) (n = 9). Sepsis was induced by cecal ligation and puncture after 30 days of A. faecalis A12C pretreatment or without. SA group had a higher survival rate of 58% vs. 16% for SC group (P < 0.05). Overall, AGUIA showed better status than AGUIC (P < 0.01). Higher monocytosis was found in AGUIA and AGUSTO vs. AGUIC and AGUSAN, respectively (P < 0.05). A gradual increase in curdlan fecal concentration was observed in AGUIA during pretreatment. Fecal concentrations of Escherichia coli significantly decreased in AGUIA and AGUSTO. Bacterial load in urine, peritoneal lavage fluid (PLF), and bronchoalveolar lavage fluid (BALF) decreased (P < 0.05) in AGUIA vs. AGUIC. Finally, lower inflammation was observed in serum, BALF, and PLF, with reduced IL-6, IL-10, IL-1β, and TNF-α, along with less damage in lungs and peritoneum in AGUIA vs. AGUIC. These findings suggest the connection between curdlan—produced by A. faecalis A12C—with the immune system and the reduction in severity of experimental sepsis.
Curdlan, a β-1,3/1,6-glucan found in Alcaligenes faecalis (A. faecalis) wall, activates innate and humoral immunity. The aim of this study is to evaluate whether pretreated rats with A. faecalis A12C could prevent sepsis disturbances and identify the immunomodulatory mechanisms involved. Experiments occurred in two stages: a survival study with 16 rats randomly divided into septic (SC) (n = 8) and septic pretreated (SA) (n = 8) groups and 45 rats divided into four groups: healthy (AGUSAN) (n = 9), septic (AGUIC) (n = 13), septic pretreated (AGUIA) (n = 14), and healthy pretreated (AGUSTO) (n = 9). Sepsis was induced by cecal ligation and puncture after 30 days of A. faecalis A12C pretreatment or without. SA group had a higher survival rate of 58% vs. 16% for SC group (P < 0.05). Overall, AGUIA showed better status than AGUIC (P < 0.01). Higher monocytosis was found in AGUIA and AGUSTO vs. AGUIC and AGUSAN, respectively (P < 0.05). A gradual increase in curdlan fecal concentration was observed in AGUIA during pretreatment. Fecal concentrations of Escherichia coli significantly decreased in AGUIA and AGUSTO. Bacterial load in urine, peritoneal lavage fluid (PLF), and bronchoalveolar lavage fluid (BALF) decreased (P < 0.05) in AGUIA vs. AGUIC. Finally, lower inflammation was observed in serum, BALF, and PLF, with reduced IL-6, IL-10, IL-1β, and TNF-α, along with less damage in lungs and peritoneum in AGUIA vs. AGUIC. These findings suggest the connection between curdlan—produced by A. faecalis A12C—with the immune system and the reduction in severity of experimental sepsis.
Curdlan, a β-1,3/1,6-glucan found in Alcaligenes faecalis (A. faecalis) wall, activates innate and humoral immunity. The aim of this study is to evaluate whether pre-treated rats with A.faecalis A12C could prevent sepsis disturbances and identify the immunomodulatory mechanisms involved. Experiments occurred in two stages: a survival study with 16 rats randomly divided into septic (SC) (n = 8) and septic pre-treated (SA) (n = 8) groups; and 45 rats divided into four groups: healthy (AGUSAN) (n = 9), septic (AGUIC) (n = 13), septic pre-treated (AGUIA) (n = 14), and healthy pre-treated (AGUSTO) (n = 9). Sepsis was induced by cecal ligation and puncture after 30 days of A.faecalis A12C pre-treatment or without. SA group had a higher survival rate (58%) vs SC group (16%) (P < 0.05). Overall, AGUIA showed better status than AGUIC (P < 0.01). Higher monocytosis was found in AGUIA and AGUSTO vs AGUIC and AGUSAN, respectively (P < 0.05). A gradual increase in curdlan fecal concentration was observed in AGUIA during pre-treatment. Fecal concentrations of E. coli significantly decreased in AGUIA and AGUSTO. Bacterial load in urine, peritoneal, and bronchoalveolar lavage fluids (PLF and BALF) decreased (P < 0.05) in AGUIA vs AGUIC. Finally, lower inflammation was observed in serum, BALF, and PLF, with reduced IL-6, IL-10, IL-1β, and TNF-α, along with less damage in lungs and peritoneum in AGUIA vs AGUIC. These findings suggest the connection between curdlan -produced by A. faecalis A12C- with the immune system and the reduction in severity of experimental sepsis.
Beta-lactamase is an enzyme protein that plays a role in the occurrence of antibiotic resistance against Methicillin-resistant Staphylococcus aureus (MRSA) bacteria. This study aims to investigate interactions that occur beta-glucan with Beta-lactamase enzymes and Protein Binding Penicillin-2a (PBP-2a). In this study, the bioinformatics approach or in-silico method was conducted to determine the molecular interactions that occurred computationally. The protein used was Beta-lactamase protein (4ooy), and Protein Binding Penicillin-2a (6h50) obtained from the Protein Data Bank. Beta-glucan as ligand obtained from the PubChem web server. Protein stabilization was carried out to adjust to the body's physiology, carried out using Pymol by removing water atoms and adding hydrogen atoms. Pharma expert web server and Pyrex were used to modulate the interaction between ligand and enzyme. We were analyzed molecular interactions visualization on the molecular complexes generated by docking simulations using the Discovery Studio software. The results showed that beta-glucan has high activity as an antibiotic against Beta-lactamase and PBP-2a. The binding affinity interaction that occurs between Beta-glucan and Beta-lactamase complex interaction was -11.1 kcal/mol, while Beta-glucan and BPP-2a was -8.5 kcal/mol. The interaction bond Beta-glucan and Beta-lactamase was higher than 2s, 5r) -1-Formyl-5 - [(Sulfooxy) amino] piperidine-2-Carboxamid as control ligand. Beta-glucan was predicted to have strong antibacterial properties. However, exploration of beta-glucan compounds and further research to determine the antibacterial effect of beta-glucan against MRSA bacteria.
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