3: LPS interaction with CNS:
(LPS not only induces inflammation into the brain, it also can interact directly with neurotransmitter activity.)
1: Immunology. 2004 Oct;113(2):224-33.
Histamine induces Toll-like receptor 2 and 4 expression in endothelial cells and
enhances sensitivity to Gram-positive and Gram-negative bacterial cell wall
components.
Talreja J, Kabir MH, B Filla M, Stechschulte DJ, Dileepan KN.
Division of Allergy, Clinical Immunology, and Rheumatology, Department of
Medicine, The University of Kansas Medical Center, Kansas City, KS, USA.
jtalreja@kumc.edu
Histamine is a major inflammatory molecule released from the mast cell, and is
known to activate endothelial cells. However, its ability to modulate
endothelial responses to bacterial products has not been evaluated. In this
study we determined the ability of histamine to modulate inflammatory responses
of endothelial cells to Gram-negative and Gram-positive bacterial cell wall
components and assessed the role of Toll-like receptors (TLR) 2 and 4 in the
co-operation between histamine and bacterial pathogens. Human umbilical vein
endothelial cells (HUVEC) were incubated with lipopolysaccharide (LPS),
lipoteichoic acid (LTA), or peptidoglycan (PGN) in the presence or absence of
histamine, and the expression and release of interleukin-6 (IL-6), and NF-kappaB
translocation were determined. The effect of histamine on the expression of mRNA
and proteins for TLR2 and TLR4 was also evaluated. Incubation of HUVEC with LPS,
LTA and PGN resulted in marked enhancement of IL-6 mRNA expression and IL-6
secretion. Histamine alone markedly enhanced IL-6 mRNA expression in HUVEC, but
it did not stimulate proportional IL-6 release. When HUVEC were incubated with
LPS, LTA, or PGN in the presence of histamine marked amplification of both IL-6
production and mRNA expression was noted. HUVEC constitutively expressed TLR2
and TLR4 mRNA and proteins, and these were further enhanced by histamine. The
expression of mRNAs encoding MD-2 and MyD88, the accessory molecules associated
with TLR signalling, were unchanged by histamine treatment. These results
demonstrate that histamine up-regulates the expression of TLR2 and TLR4 and
amplifies endothelial cell inflammatory responses to Gram-negative and
Gram-positive bacterial components.
PMID: 15379983 [PubMed - indexed for MEDLINE]
(Sensitized individuals are not only at risk from acute infections but are also exposed to a steady micro-dose of LPS from resident bacteria. In addition to these, there are other chronic exposures.)
4: LPS and dental disease as constant source:
1: Life Sci. 2006 Mar 20;78(17):2012-8. Epub 2005 Nov 14.
Lipopolysaccharide stimulates the production of prostaglandin E2 and the
receptor Ep4 in osteoblasts.
Shoji M, Tanabe N, Mitsui N, Tanaka H, Suzuki N, Takeichi O, Sugaya A, Maeno M.
Department of Oral Health Sciences, Nihon University School of Dentistry,
1-8-13, Kanda Surugadai, Tokyo 101-8310, Japan.
Previous studies have indicated that one of the causes of alveolar bone
destruction with periodontitis is lipopolysaccharide (LPS) from the cell wall of
gram-negative bacteria in plaque, and that prostaglandin E(2) (PGE(2)) is one of
the bone resorption factors that stimulate osteoclast formation through an
intercellular interaction between osteoblasts and osteoclast precursors. The
present study was undertaken to determine the effect of LPS on cell growth,
alkaline phosphatase (ALPase) activity, the production of PGE(2), and the
expression of receptors by PGE(2), cyclooxygenase (COX)-1, and COX-2, using
human osteosarcoma cell line Saos-2 as osteoblasts. The cells were cultured with
0, 1, or 10 microg mL(-1) of LPS for up to 14 days. The production of PGE(2) and
the gene expression of COX-1, COX-2, and PGE(2) receptors, including Ep1, Ep2,
Ep3, and Ep4, were determined using enzyme-linked immunosorbent assay (ELISA)
and real-time reverse transcription-polymerase chain reaction (real-time
RT-PCR), respectively. With the addition of LPS, cell growth and ALPase activity
decreased by day 5 of the culture, while PGE(2) production increased in a
dose-dependent manner throughout the entire 14-day culture period. LPS-reduced
ALP activity and LPS-induced PGE(2) production returned to the control level by
the addition simultaneously with indomethacin. The expression of COX-1, Ep1,
Ep2, and Ep3 receptors decreased on day 14 of the culture, whereas the
expression of COX-2 and Ep4 receptors increased significantly with the addition
of LPS. These results suggest that LPS promotes PGE(2) production by increasing
the expression of COX-2, and that LPS promotes the production of Ep4 receptors
in osteoblasts. These results also indicate that LPS-induced PGE(2) may combine
with osteoblast Ep4 receptors in autocrine or paracrine modes, and may promote
the formation of osteoclasts.
PMID: 16289620 [PubMed - indexed for MEDLINE]
5: LPS and house dust as constant source:
1: Arh Hig Rada Toksikol. 2004 Jun;55(2-3):175-81.
Endotoxin measurement in house dust using the end-point Limulus amoebocyte
lysate method.
Varnai VM, Macan J, Plavec D, Juresa D.
Institute for Medical Research and Occupational Health, Zagreb, Croatia.
vvarnai@imi.hr
Endotoxin is a lipopolysaccharide, a part of gram-negative bacteria cell
membrane commonly present in general and many occupational environments. This
paper describes sample preparation and endotoxin measurement in 16 samples of
house dust from urban homes (Zagreb, Croatia) using end-point chromogenic
Limulus amoebocyte lysate (LAL) bioassay. House dust was collected on cellulose
filters by vacuuming bedroom and living room floors, and was kept frozen until
assayed. Samples were extracted from filters with a 0.05% solution of Tween-20
in endotoxin-free water. Serial dilutions of samples were measured in
duplicates. The linearity of the standard curve was satisfying (r=0.983), as
well as the recovery (92 and 110%) and repeatability (coefficient of variation
from 0 to 8.5%). The endotoxin levels found in the house dust samples ranged
from 4.8 to 200 EU/mg, with the arithmetic mean of 49.5 EU/mg (standard error of
the mean of 12.1 EU/mg), and were in the range of house dust endotoxin values
obtained by other authors.
PMID: 15285466 [PubMed - indexed for MEDLINE]
(Gram-negative bacteria and their exaggerated response to certain antibiotics can result in an acute crisis as endotoxin levels are quickly raised.)
6: LPS and amplification of endotoxin output by targeted bacteria:
1: Folia Microbiol (Praha). 2005;50(2):167-71.
Antibiotic-induced release of inflammatory mediators from bacteria in
experimental Klebsiella pneumoniae-induced sepsis.
Toky V, Sharma S, Bramhne HG, Chhibber S.
Department of Microbiology, Panjab University, 160 014 Chandigarh, India.
kltoky@yahoo.com
In a fibrin-clot model of sepsis, developed in mice, treatment with the
antibiotics ceftazidime (Cfz) and ofloxacin (Ofl) caused significant (p < 0.01)
release of endotoxin and TNF-alpha after 4.5 h when compared with control
(untreated) and amikacin (Ami) treated group. Except for control group, the
level of bacteremia declined in all three antibiotic-treated groups. The results
suggest that antibiotic therapy, irrespective of the agent used, results in an
increase in endotoxin levels in vivo. The amount of endotoxin liberated by Ami
was much smaller than with Cfz and Ofl therapy, which makes it an appropriate
agent for the treatment of sepsis. An increase in the level of TNF-alpha along
with endotoxin is suggestive of increased inflammatory response.
PMID: 16110923 [PubMed - indexed for MEDLINE]