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

@article{Dery2004FrontlineIO,
  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},
  year={2004},
  volume={34}
}
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… 
View on Wiley
ncbi.nlm.nih.gov
37 Citations
Highly Influential Citations
2
Background Citations
19
Methods Citations
5

37 Citations

The tripeptide feG regulates the production of intracellular reactive oxygen species by neutrophils

FeG reduces the capacity of circulating neutrophils to generate intracellular ROS consequent to an allergic reaction by preventing the deregulation of PKCδ.

feG-COOH blunts eosinophilic airway inflammation in a feline model of allergic asthma

Data indicate that a single dose of feG-COOH partially attenuates eosinophilic airway inflammation in experimental feline asthma.

Chronic use of the immunomodulating tripeptide feG-COOH in experimental feline asthma.

Effects of the recombinant allergen rDer f 2 on neuro-endocrino-immune network in asthmatic mice

In brief, recombinant allergen Der f 2 can strengthen the function of hypothalamus-pituitary-adrenal (HPA) axis, affect the balance of Th1 and Th2 cytokines, and reduce pulmonary inflammation in asthmatic mice.

Prevention and amelioration of rodent endotoxin-induced lung injury with administration of a novel therapeutic tripeptide feG.

Tripeptide feG prevents and ameliorates acute pancreatitis-associated acute lung injury in a rodent model.

FeG reduced leukocyte infiltration, ameliorated the severity of inflammatory damage, and restored lung function when administered either prophylactically or therapeutically in a two-hit rat model of acute pancreatitis plus intratracheal lipopolysaccharide.

Treatments for Pulmonary Ricin Intoxication: Current Aspects and Future Prospects

The only post-exposure measure that is effective against pulmonary ricinosis at clinically relevant time-points following intoxication in pre-clinical studies is passive immunization with anti-ricin neutralizing antibodies, which depends on antibody affinity and the time of treatment initiation within a limited therapeutic time window.

The tripeptide analog feG ameliorates severity of acute pancreatitis in a caerulein mouse model.

It is concluded that feG ameliorates experimental AP acting at least in part by modulating ICAM-1 expression in the pancreas.

Salivary gland derived peptides as a new class of anti-inflammatory agents: review of preclinical pharmacology of C-terminal peptides of SMR1 protein

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.

References

SHOWING 1-10 OF 38 REFERENCES

Submandibular gland peptide‐T (SGP‐T): Modulation of endotoxic and anaphylactic shock

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

The severity of pulmonary inflammation initiated by systemic anaphylaxis is depressed by bilateral ganglionectomy or decentralization of SCG, and the increases in levels of serum-derived proteins, histamine, and influx of cells observed in BALF after anphylaxis were attenuated by both decentralization and ganglions.

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

The inhibition by these tripeptides on neutrophil adhesion to myocytes suggests that salivary glands hormones regulate the severity of cardiac inflammation.

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.

Attenuation of intestinal and cardiovascular anaphylaxis by the salivary gland tripeptide FEG and its d-isomeric analog feG

Role for the submandibular gland in modulating pulmonary inflammation following induction of systemic anaphylaxis

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

The data suggest that activated T cells may be involved in the regulation of allergen-induced AHR in a relevant animal model of allergic asthma.

Submandibular Gland Peptide-T (SGP-T) Inhibits Intestinal Anaphylaxis

Results emphasize that modulation of immediate hypersensitivity reactions is only one ofseveral gastrointestinal activities that are affected by growth factors and peptides released from salivary glands.

Role of intercellular adhesion molecule-1 in antigen-induced lung inflammation in brown Norway rats.

It is concluded that ICAM-1 is critically important for the antigen-specific recruitment of eosinophils and lymphocytes into the lungs and in association with a reduced inflammatory pathology in lung tissue.

Immunophenotyping of eosinophils recovered from blood and BAL of allergic asthmatics.

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.