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The effects of beta‐glucan treatment on endotoxin and sepsis‐induced cytokine production
Author(s) -
Newsome Courtni Takiyah,
LeBlanc Brian,
Ayala Alfred,
Reichner Jonathan
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.439.1
Subject(s) - glucan , cytokine , sepsis , immune system , tumor necrosis factor alpha , in vivo , inflammation , medicine , lipopolysaccharide , immunology , pharmacology , chemistry , biology , biochemistry , microbiology and biotechnology
β‐glucans, a class of glucose polymers found in the fungal cell wall, stimulate innate immune cells. Stimulating immune cell function can be of clinical benefit; however, it often causes the overproduction of inflammatory cytokines. The soluble β‐glucan, PGG‐β ‐glucan, primes antimicrobial functions without inducing cytokines. In vitro studies have tested whether the lack of cytokine production is due to a suppressor mechanism. These studies indicated that β‐glucan pretreatment reduces LPS‐induced TNF production. The aims of this project were 1) to evaluate the effect of β‐glucan pretreatment on the LPS‐induced TNF production in vivo and 2) to evaluate the effect of β‐glucan on IL‐6 production in septic mice induced by cecal ligation and puncture when given after the onset of infection. During this study, the age and sex of the mice and the time of β‐glucan administration were varied. After the administration of LPS or the onset of sepsis, serum TNF and IL‐6 levels were measured by ELISA. The results indicate that β‐glucan pretreatment reduces LPS‐induced TNF production and that there is a possible age‐response. The results also indicate that β‐glucan given after the onset of sepsis reduces IL‐6 and that the effect may be sex‐specific. The development of β‐glucan as a therapeutic agent with negligible side effects could aid patients with uncontrolled inflammation. NIH R01‐GM066194 (JR) and NIH F31‐GM086069 (CN)