Sepsis – Oxidative Stress: Prauchner CA, “Oxidative stress in sepsis: Pathophysiological implications justifying antioxidant co-therapy;”Burns, pii:S0305-4179(16)30400-4. PMID 28034666; Dec 26, 2016. Quote: Sepsis is one of the main causes of death among critically ill patients. Sepsis pathogenesis includes infection by gram-negative and gram-positive bacteria, fungi, or both; exacerbated inflammatory response; hypotension, with potential to cause vasodilatory shock; and lesser delivery of oxygen to tissues due to impairment of oxygen utilization by cells. Antioxidants could inhibit the over expression of iNOS [nitric oxide synthase] in sepsis. In line with this, several antioxidants such as vitamins C and E, polyphenols, melatonin, β-glucan, N-acetylcysteine, mitochondrion-targeted antioxidants (MitoQ, MitoE, and peptides associated with dimethyltyrosine), selenium salts, and organoselenium compounds were effective in ameliorating oxidative stress in animal models of sepsis and in a number of clinical trials with septic patients.
Sepsis-Intraabdominal: Tzianabos AO, Cisnerol RL, et al; “Protection against intra-abdominal sepsis by two polysaccharide immonumodulators (Beta 1,3/1,6 glucan),” J Infect Dis, 178:1,200-6. 1998. Quote: “These data demonstrate the usefulness of [Beta 1,3/1,6 glucan]… in preventing experimental intraabdominal sepsis…and may represent a new adjunct to antibiotic regimens currently used to prevent clinical cases of this disease”
Sepsis-Pneumoniae: Vural K, et al, “Investigation of the protective effects of beta-D-glucan against invasive encapsulated Streptococcus pneumoniae sepsis in splenectomized rats,” Mikrobiyol Bul, Jul;49(3): 314-26, 2015.PMID 26313274-PubMed in Progress. Quote: “The most common species which are responsible for sepsis are encapsulated bacteria such as Streptococcus pneumoniae, Haemophilus influenzae and Neisseria meningitidis. …b-D-glucan[BDG] … shows immunomodulatory activity, by enhancing the resistance of the host against microbial agents, and promotes phagocytic and proliferative activities of reticuloendothelial system [phagocytic cells including macrophages and monocytes involved in the immune system]. …BDG, ceftriaxone and BDG+ceftriaxone groups had statistically significant decrease in the amount of bacteria in all tissues when compared to the sepsis group (p<0.05). … The data of our study suggests that, BDG [B-D-glucan]alone, an immunomodulatory agent, alone and in combination with ceftriaxone can reverse the systemic inflammatory reaction in Streptococcus pneumoniae sepsis and thereby can reduce multiple organ failure.”
Sepsis – Pneumonia: Maurici da Rocha e Silva et al; “Infection Prevention in Patients with Severe Multiple Trauma with the Immunomodulater Beta 1-3 Polyglucose (glucan);” Surgery, Gynecology & Obstetrics; 177:383-388. 1993. Quote: “The incidence of hospital pneumonia of 55% and sepsis of 35% confirms results of previous studies of patients with multitrauma. Glucan decreased pneumonia and sepsis to a significantly lower level of 9.5%….The mortality rate related to infection decreased from 30.0 to 4.8%. The lower number of instances of pneumonia and sepsis….decreased the period of time in the intensive care and the hospital, with a global reduction of 40% on hospital cost.”
Sepsis: Sener G, Toklu H, et al; “Protective effect of beta-glucan against oxidative organ injury in a rat model of sepsis,” Int Immunopharmacol:1387-96 Epub 2005/Aug 2005. Quote: “Sepsis leads to various organ damage and dysfunction. One of the underlying mechanisms is thought to be oxidative damage due to generation of free radicals. …Elevated plasma TNF-alpha levels in septic rats [was] significantly reduced to control levels in beta-glucan treated rats. Since beta-glucan administration reversed these oxidant responses, it seems likely that beta-glucan protects against sepsis-induced oxidative organ injury.”
Sepsis Associated Lung Damage – Sepsis: Babayigit H, Kucuk C, Sozuer E, Yazici C, Kose K, Akgun H.; “Protective effect of beta-glucan on lung injury after cecal ligation and puncture in rats.” Department of General Surgery, School of Medicine, Erciyes University, 38039, Kayseri, Turkey; Intensive Care Med. (6):865-70; Jun 31, 2005. Quote: “In this rat model of intra-abdominal sepsis beta-glucan treatment partially protected against secondary lung injury, decreased lung hemorrhages, and lung neutrophilia. These results suggest that beta-glucan protects against sepsis-associated lung damage.”
Sepsis pneumoccoccal: Browder W, Williams D, Di Luzio N, et al, “Protective effect of nonspecific immunostimulation in postsplenectomy sepsis,” J Surg Res, Dec:35(6):474-9, 1983 PMID 6656237. Quote: “This study reports the use of glucan, a beta-1,3-polyglucose, as a nonspecific immunostimulant for postsplenectomy pneumococcal sepsis. ,,, Glucan significantly increased survival in the splenectomy group (75%) compared to controls (27%). … Nonspecific immunostimulation [by a beta-1,3-polyglucose] appears to have significant potential as a treatment strategy against postsplenectomy infection.”
Septic Shock: Williams D.L. ,et al; “The role of complement in glucan-induced protection against septic shock.” Circ. Shock. 25:53-60. 1988