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Complement C5a receptors in the pituitary gland: expression and function.

Karen Francis¹, B Mary Lewis, Peter N Monk

¹Centre for Endocrine and Diabetes Sciences, Cardiff University, Cardiff, CF14 4XN, UK.

The Journal of Endocrinology

|November 21, 2008

Summary

This summary is machine-generated.

The anterior pituitary gland contains C5a receptors that can reduce inflammation. These receptors inhibit macrophage migration inhibitory factor (MIF) release and stimulate ACTH secretion, suggesting a role in immune-endocrine communication.

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Area of Science:

Neuroendocrinology
Immunology
Cellular Signaling

Background:

The hypothalamic-pituitary-adrenal axis regulates inflammation via immune-endocrine communication.
The innate immune system releases anaphylatoxins like C5a in response to pathogens.
C3a receptors exist in the anterior pituitary; C5a receptor presence was investigated.

Purpose of the Study:

To investigate the presence and function of C5a receptors in the rat anterior pituitary gland.
To determine the effects of C5a and its derivative C5adR on inflammatory and hormonal pathways.
To explore the role of C5a receptors in modulating inflammation and hormone secretion.

Main Methods:

RT-PCR and immunocytochemistry to detect C5a receptors and C5L2.
Western blotting to analyze MAPK, AKT, and p38 phosphorylation.
ELISA to measure macrophage migration inhibitory factor (MIF) secretion.
Assessment of ACTH secretion from AtT-20DV16 cells.

Main Results:

C5a receptors and C5L2 were identified in the rat anterior pituitary and cell lines.
C5a stimulated MAPK and AKT phosphorylation, while C5adR had no effect.
Both C5a and C5adR dose-dependently inhibited MIF release (IC50 ≈ 20 nM).
C5a and C5adR stimulated ACTH secretion from AtT-20DV16 cells (up to 25%).

Conclusions:

Functional C5a receptors (C5a and C5L2) are present in the anterior pituitary gland.
C5a receptor activation inhibits MIF release, suggesting an anti-inflammatory role.
C5a receptor activation stimulates ACTH release, indicating involvement in neuroendocrine responses.