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» LymeNet Flash » Questions and Discussion » Medical Questions » Peptide-T in recent studies again for non-inflammatory

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Author Topic: Peptide-T in recent studies again for non-inflammatory
Dawn in VA
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Those familiar w/Candance Pert's work will know what I'm yapping about.

Some basic info from good ole' Wikipedia:

Early work in identifying factors that played a role in the CST-SMG axis lead to the discovery of a seven amino acid peptide, called the submandibular gland peptide-T. SGP-T was demonstrated to have biological activity and thermoregulatory properties related to endotoxin exposure.[7] SGP-T, an isolate of the submandibular gland, demonstrated its immunoregulatory properties and potential role in modulating the cervical sympathetic trunk-submandibular gland (CST-SMG) axis, and subsequently was shown to play an important role in the control of inflammation.

One SGP-T derivative is a three-amino acid sequence shown to be a potent anti-inflammatory molecule with systemic effects. This three-amino acid peptide is phenylalanine-glutamine-glycine (FEG) and its D-isomeric form (feG) have become the foundation for the ImSAID category.[8]

Cellular Effects of feG: The cellular effects of the ImSAIDs are characterized in a number of publications. feG and related peptides are known to modulate leukocyte (white blood cells) activity by influencing cell surface receptors to inhibit excessive activation and tissue infiltration.
One lead ImSAID, the tripeptide FEG (Phe-Glu-Gly) and its D-isomer feG are known to alter leukocyte adhesion involving actions on αMβ2 integrin, and inhibit the binding of CD16b (FCyRIII) antibody to human neutrophils.[9]

feG has also been shown to decrease circulating neutrophil and eosinophil accumulation, decrease intracellular oxidative activity, and reduce the expression of CD49d after antigen exposure.[10][11][12]


Some advocate the consumption of anti-inflammatory foods as a means of controlling inflammation. A typical anti-inflammatory diet includes a well-balanced, varied diet that is high in vegetables and low in refined carbohydrates and undesirable fats, such as saturated fats and trans fats.[17] Anti-inflammatory foods include most colorful fruits and vegetables, oily fish (which contain higher levels of omega-3 fatty acids), nuts, seeds, and certain spices, such as ginger.

***Blah blah blah, we know that already, but the molecular reasons behind it all were enlightening (at least for me).*** See more below:

***Extra-virgin olive oil contains the chemical oleocanthal that acts similarly to ibuprofen.***

Those following an anti-inflammatory diet will avoid refined oils and sugars, and show a preference for so-called anti-inflammatory foods in their meal choices.[18]

A diet high in vegetables and low in refined carbohydrates and saturated and trans fats may enhance the creation of prostaglandins. There are three main types of prostaglandins: PG-E1 and PG-E3, which have an anti-inflammatory properties, and PG-E2, which promotes inflammation.[citation needed]

Omega-3 fatty acids have been shown to disrupt inflammation cell signaling pathways by binding to the GPR120 receptor.[19]

^ Ottani A, Leone S, Sandrini M, Ferrari A, and Bertolini A (2006) The analgesic activity of paracetamol is prevented by the blockade of cannabinoid CB1 receptors. Eur J Pharmacol 531: 280-281.
^ The local antinociceptive effects of paracetamol in neuropathic pain are mediated by cannabinoid receptors. Mlina Dania, Jose Guindona, Chantal Lamberta and Pierre Beaulieu
^ a b c NSAIDs and adverse effects at Bandolier, Table 7.
^ Bao F, John SM, Chen Y, Mathison RD, Weaver LC. The tripeptide phenylalanine-(D) glutamate-(D) glycine modulates leukocyte infiltration and oxidative damage in rat injured spinal cord. Neuroscience. 2006 Jul 7;140(3):1011-22. Epub 2006 Apr 3.
^ Mathison RD, Befus AD, Davison JS, Woodman RC. Modulation of neutrophil function by the tripeptide feG. BMC Immunol. 2003 Mar 4;4:3. Epub 2003 Mar 4
^ Mathison R, Davison JS, Befus AD. Neuroendocrine regulation of inflammation and tissue repair by submandibular gland factors. Immunol Today. 1994 Nov;15(11):527-32. Review.
^ Mathison RD, Malkinson T, Cooper KE, Davison JS. Submandibular glands: novel structures participating in thermoregulatory responses. Can J Physiol Pharmacol. 1997 May;75(5):407-13.
^ Dery RE, Mathison R, Davison J, Befus AD. Inhibition of allergic inflammation by C-terminal peptides of the prohormone submandibular rat 1 (SMR-1). Int Arch Allergy Immunol. 2001 an-Mar;124(1-3):201-4.
^ Mathison RD, Christie E, Davison JS. The tripeptide feG inhibits leukocyte adhesion. J Inflamm (Lond). 2008 May 20;5:6.
^ Dery RE, Ulanova M, Puttagunta L, Stenton GR, James D, Merani S, Mathison R, Davison J, Befus AD. Frontline: Inhibition of allergen-induced pulmonary inflammation by the tripeptide feG: a mimetic of a neuro-endocrine pathway. Eur J Immunol. 2004 Dec;34(12):3315-25
^ Mathison RD, Davison JS. The Tripeptide feG Regulates the Production of Intracellular Reactive Oxygen Species by Neutrophils. J Inflamm (Lond). 2006 Jun 15;3(1):9
^ Mathison R, Lo P, Tan D, Scott B, Davison JS. The tripeptide feG reduces endotoxin-provoked perturbation of intestinal motility and inflammation. Neurogastroenterol Motil. 2001 Dec;13(6):599-603.
^ Harv Ment Health Lett. 2008 Aug;25(2). Anti-inflammatory drugs may not protect cognitive function
^ Rogers J., J Periodontol. 2008 Aug;79(8 Suppl):1535-43. The inflammatory response in Alzheimer's disease'
^ Sano M, Grossman H, Van Dyk K, CNS Drugs. 2008;22(11):887-902, Preventing Alzheimer's disease : separating fact from fiction.
^ Hyman, Mark: "Ultra-Metabolism", page 137. Scribner, 2006
^ [1]

(The ole disclaimer: I'm not a doctor.)

Posts: 1349 | From VA | Registered: Jul 2006  |  IP: Logged | Report this post to a Moderator

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