PMID- 9864222
OWN - NLM
STAT- MEDLINE
DCOM- 19990128
LR  - 20240314
IS  - 0019-9567 (Print)
IS  - 1098-5522 (Electronic)
IS  - 0019-9567 (Linking)
VI  - 67
IP  - 1
DP  - 1999 Jan
TI  - Modulation of endotoxin- and enterotoxin-induced cytokine release by in vivo 
      treatment with beta-(1,6)-branched beta-(1,3)-glucan.
PG  - 244-52
AB  - Leukocytes activated by endotoxin or enterotoxins release proinflammatory 
      cytokines, thereby contributing to the cascade of events leading to septic shock. 
      In the present studies, we analyzed the effects of in vivo administration of a 
      soluble immunomodulator, beta-(1,6)-branched beta-(1,3)-glucan (soluble 
      beta-glucan), on toxin-stimulated cytokine production in monocytes and 
      lymphocytes isolated from treated mice. In vitro stimulation of lymphocytes 
      isolated from soluble beta-glucan-treated mice with lipopolysaccharide (LPS) 
      resulted in enhanced production of interleukin-6 (IL-6) and suppressed production 
      of tumor necrosis factor alpha (TNF-alpha), while stimulation of these cells with 
      staphylococcal enterotoxin B (SEB) or toxic shock syndrome toxin 1 (TSST-1) 
      resulted in enhanced production of gamma interferon (IFN-gamma) and suppressed 
      production of IL-2 and TNF-alpha compared to that in cells isolated from 
      untreated mice. In vitro stimulation of monocytes isolated from soluble 
      beta-glucan-treated mice with LPS also resulted in suppressed TNF-alpha 
      production, while stimulation of these cells with SEB or TSST-1 resulted in 
      suppressed IL-6 and TNF-alpha production compared to that in cells isolated from 
      untreated mice. Thus, the overall cytokine pattern of leukocytes from soluble 
      beta-glucan-treated mice reflects suppressed production of proinflammatory 
      cytokines, especially TNF-alpha. Taken together, our results suggest that 
      treatment with soluble beta-glucan can modulate the induction cytokines during 
      sepsis, resulting in an overall decrease in host mortality.
FAU - Soltys, J
AU  - Soltys J
AD  - Department of Veterinary Molecular Biology, Montana State University, Bozeman 
      59717, USA.
FAU - Quinn, M T
AU  - Quinn MT
LA  - eng
GR  - S10 RR11877/RR/NCRR NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Infect Immun
JT  - Infection and immunity
JID - 0246127
RN  - 0 (Adjuvants, Immunologic)
RN  - 0 (Bacterial Toxins)
RN  - 0 (Cytokines)
RN  - 0 (Enterotoxins)
RN  - 0 (Glucans)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Superantigens)
RN  - 0 (beta-Glucans)
RN  - 0 (enterotoxin F, Staphylococcal)
RN  - 37361-00-5 (beta-1,6-glucan)
RN  - 39424-53-8 (enterotoxin B, staphylococcal)
RN  - 9051-97-2 (beta-1,3-glucan)
SB  - IM
MH  - Adjuvants, Immunologic/administration & dosage
MH  - Animals
MH  - Apoptosis/drug effects/immunology
MH  - *Bacterial Toxins
MH  - Cytokines/*metabolism
MH  - Enterotoxins/*pharmacology
MH  - Female
MH  - Glucans/*administration & dosage
MH  - Injections, Intramuscular
MH  - Lipopolysaccharides/*pharmacology
MH  - Lymphocytes/immunology/metabolism
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Monocytes/immunology/metabolism
MH  - Staphylococcus aureus/immunology
MH  - Superantigens/pharmacology
MH  - *beta-Glucans
PMC - PMC96303
EDAT- 1998/12/24 00:00
MHDA- 1998/12/24 00:01
PMCR- 1999/01/01
CRDT- 1998/12/24 00:00
PHST- 1998/12/24 00:00 [pubmed]
PHST- 1998/12/24 00:01 [medline]
PHST- 1998/12/24 00:00 [entrez]
PHST- 1999/01/01 00:00 [pmc-release]
AID - 0632 [pii]
AID - 10.1128/IAI.67.1.244-252.1999 [doi]
PST - ppublish
SO  - Infect Immun. 1999 Jan;67(1):244-52. doi: 10.1128/IAI.67.1.244-252.1999.