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INNATE IMMUNITY 3
TLR2 Agonists
FSL-1 - TLR2/6 Agonist
FSL-1 (Pam2CGDPKHPKSF) is a synthetic lipoprotein derived from Mycoplasma salivarium similar to MALP-2, a M. fermentans derived lipopeptide (LP) 1,2 .
Mycoplasmal LPs, such as FSL-1, contain a diacylated cysteine residue, whereas bacterial LP contain a triacylated one. FSL-1 is recognized by TLR2 and TLR6,
whereas bacterial LPs are recognized by TLR2 and TLR1 3 .
HKAL (Acholeplasma laidlawii)
Acholeplasma laidlawii, a member of the mycoplasma family, is a cell wall-less bacteria. Heat killed mycoplasma such as HKAL induce higher stimulation of
macrophage than lipoproteins from Gram- bacteria, even at low concentrations 4 . This response is mediated by TLR2 and MyD88.
HKEB (Escherichia coli) NEW
HKEB is a heat killed preparation of the gram negative bacterium, E.coli O111:B4. Cell wall components from this bacterium, such as peptidoglycan (PGN)
and lipopolysaccharide (LPS), are recognized by TLR2 and TLR4 5 . It has been demonstrated that HKEB can stimulate TLR2 and induce the production of
NF-kB and pro-inflammatory cytokines, such as IL-8 6 . HKEB is a potent stimulator of TLR2, and has a weak stimulatory effect on TLR4.
HKHP (Helicobacter pylori)
Helicobacter pylori, a Gram negative bacterium, is an important human pathogen that causes gastritis and is strongly associated with peptic ulcer, gastric
adenocarcinoma, and mucosa-associated lymphoid tissue lymphoma. Heat-killed Helicobacter pylori (HKHP) induces the production of IL-8 through the
activation of the ERK and p38 MAPK pathway. TLR2 was shown to be the sensor involved in HKHP-mediated secretion of IL-8 in monocytes 7 .
HKLM (Listeria monocytogenes)
HKLM is a freeze-dried heat-killed preparation of Listeria monocytogenes (LM), a facultative intracellular Gram-positive bacterium. Infection with LM induces
the secretion of inflammatory cytokines, such as TNF, IL-12, and several chemokines, allowing the recruitment and activation of immune cells. This response
is mediated mainly by the interaction between MyD88 and TLR2 8, 9 .
HKLP (Legionella pneumophila)
Legionella pneumophila, a Gram negative bacterium, is the causative agent of legionnaires’ disease which is characterized by severe pneumonia. Although
TLR4 is involved in host defense against gram negative bacteria infection, it is not activated or is activated only to a limited extent by L. pneumophila 10 .
L. pneumophila requires TLR2 rather than TLR4 to induce the production of cytokines 11 .
HKLR (Lactobacillus rhamnosus)
Lactobacillus rhamnosus is a nonpathogenic gram-positive inhabitant of the human microflora. It is used as a natural preservative in yogurt and other dairy products
to extend the shelf life. L. rhamnosus is known to have health beneficial effects, such as the nonspecific enhancement of the immune system. Indeed, heat-killed
L.. rhamnosus (HKLR) has been shown to be a potent inducer of TNF-a from mouse mononuclear cells. This immune response is dependent on TLR2 and CD14 12 .
HKMF (Mycoplasma fermentans) NEW
Mycoplasma fermentans, a member of the mycoplasma family, is a cell wall-less bacterium. It contains lipopeptides, in particular 2-kDa macrophage-activating
lipopetide (MALP-2), a potent stimulator of macrophages through TLR2 and TLR6 3 . Stimulation with heat killed M. fermentans (HKMF) induces rapid activation
of NF-kB and the production of pro-inflammatory cytokines.
HKPA (Pseudomonas aeruginosa)
Pseudomonas aeruginosa is a virulent gram-negative pathogen that infects patients through the respiratory tract, in particular patients with cystic fibrosis.
Heat-killed Pseudomonas aeruginosa (HKPA) initiates host inflammatory responses through TLR2 and TLR5 but not TLR4 13, 14 . The TLR5-mediated response
was shown to be induced by flagellin while LPS appears to play an important role in the TLR2-mediated response.
HKPG (Porphyromonas gingivalis)
HKPG is a freeze-dried heat-killed preparation of the periodontopathic Gram negative bacteria Porphyromonas gingivalis. In CHO cells expressing TLR2 and
CD14, exposure to HKPG induces the activation of NF-kB through TLR2. Expression of TLR4 fails to enhance the response to HKPG suggesting that either
the whole bacterial components of P. gingivalis are not recognized by TLR4 or some components of these bacteria inhibit TLR4-mediated activation 15 .
HKSA (Staphylococcus aureus)
HKSA is a lyophilized heat-killed preparation of Staphyloccocus aureus, a Gram-positive extra-cellular growing bacterium. HKSA is recognized mainly by
TLR2 16 . HKSA induces tolerance to a secondary HKSA stimulation but causes priming to LPS, suggesting a differential regulation of cytokines and chemokines
in gram-positive- and gram-negative-induced inflammatory events 17 .
HKSP (Streptococcus pneumoniae)
Streptococcus pneumoniae, a Gram positive bacterium, is the principal etiologic agent of bacterial meningitis in adults. Heat-killed Streptococcus pneumoniae
(HKSP) induce activation of NF-kB in a TLR2- and CD14-dependent manner 18 . TLR2 has been shown to play an important role in the protein- and
polysaccharide-specific type 1 IgG isotype response following immunization with HKSP 19 .
LM-MS & LAM-MS (Mycobacterium smegmatis)
Lipoarabinomannans (LAM) and lipomannans (LM) are lipoglycans found in mycobacterial cell wall. LM and LAM from the non-pathogenic Mycobacterium
smegmatis are proinflammatory molecules 20 . Both LM-MS and LAM-MS activate macrophages in a TLR2-dependent manner 21 .
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