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… 

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.

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.

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.

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.

The tripeptide feG inhibits leukocyte adhesion

When administered in vivo, feG prevents inflammation-induced reductions in cell adhesion, as well as restoring its inhibitory effect in vitro, and appears to involve actions on αMβ2 integrin, with a possible interaction with the low affinity FcγRIII receptor (CD16).

A novel biomarker associated with distress in humans: calcium-binding protein, spermatid-specific 1 (CABS1).

  • T. RitzD. Rosenfield A. Befus
  • Psychology, Biology
    American journal of physiology. Regulatory, integrative and comparative physiology
  • 2017
Calcium-binding protein spermatid-specific 1 (CABS1) is expressed in the human submandibular gland and has an anti-inflammatory motif similar to that in sub mandibular rat 1 in rats, which is readily detected in human saliva and is associated with psychological and physiological indicators of stress.

Role of cellular effectors in the emergence of ventilation defects during allergic bronchoconstriction.

The findings suggest that allergic airway inflammation is locally heterogeneous and is topographically associated with the local emergence of VDs following allergen challenge.

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.

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.

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.

IL-5 and eosinophils are essential for the development of airway hyperresponsiveness following acute respiratory syncytial virus infection.

It is concluded that in response to RSV, IL-5 is essential for the influx of eosinophils into the lung and that eosInophils in turn are critical for the development of AHR.