Frontline: Inhibition of allergen‐induced pulmonary inflammation by the tripeptide feG: a mimetic of a neuro‐endocrine pathway

  title={Frontline: Inhibition of allergen‐induced pulmonary inflammation by the tripeptide feG: a mimetic of a neuro‐endocrine pathway},
  author={René E. Déry and Marina Ulanova and Lakshmi Puttagunta and Grant R. Stenton and Deborah James and Shaheed Merani and Ronald D. Mathison and J. S. Davison and A Dean Befus},
  journal={European Journal of Immunology},
Interactions between the neuro‐endocrine system and immune system help maintain health. One interaction involves the superior cervical ganglia (SCG), which regulate the prohormone submandibular rat 1 (SMR1) produced by the submandibular gland (SMG). A peptide derived from SMR1, feG, has anti‐inflammatory activity, and modification to D‐isomer feG enhances bioactivity. We tested feG as a therapeutic agent for airways inflammation, using rats sensitized by OVA or Nippostrongylus brasiliensis (Nb… 

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Treatments for Pulmonary Ricin Intoxication: Current Aspects and Future Prospects

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The term "Immune Selective Anti-Inflammatory Derivatives" (ImSAIDs) is proposed for salivary-derived peptides to distinguish this class of agents from corticosteroids and nonsteroidal anti-inflammatory drugs.

EGF receptor activation during allergic sensitization affects IL‐6‐induced T‐cell influx to airways in a rat model of asthma

BALF from OVA‐sensitized/challenged rats induced CD4+ T‐cell migration, which was inhibited by both AG1478 treatment in vivo and neutralization of IL‐6 in vitro.



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SGP‐T may be a prototype to a family of small peptides that modulate the immunological and smooth muscle reactions to severe inflammatory (endotoxic and anaphylactic) reactions.

Marked antiinflammatory effects of decentralization of the superior cervical ganglia

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Regulation of leukocyte adhesion to heart by the tripeptides feG and feG(NH2).

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Airway hyperresponsiveness is associated with inflammatory cell infiltration in allergic brown-Norway rats.

There was a significant correlation between airway responsiveness and eosinophil recovery at 5-8 h, and at 18-24 h after allergen exposure, and there was no difference between baseline lung resistance in matched saline- or OA-challenged animals at each time point.

Airway hyperresponsiveness, elevation of serum-specific IgE and activation of T cells following allergen exposure in sensitized Brown-Norway rats.

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The finding that eosinophils in BAL are activated and can interact with T cells is further evidence for the proinflammatory role of these cells in allergic asthma.