Endotoxin-induced inflammation disturbs melatonin secretion in ewe

Area of Science:

• Reproductive endocrinology
• Neuroendocrinology
• Animal physiology

Background:

• Melatonin, a key hormone in regulating circadian rhythms, is synthesized in the pineal gland.
• Bacterial endotoxins like lipopolysaccharide (LPS) can induce inflammatory responses affecting hormonal regulation.
• Photoperiod significantly influences reproductive and endocrine functions in many species, including sheep.

Purpose of the Study:

• To investigate the impact of intravenous lipopolysaccharide (LPS) administration on nocturnal melatonin secretion in ewes.
• To assess the effect of LPS on the expression of enzymes within the melatonin biosynthetic pathway in the pineal gland.
• To determine if photoperiodic conditions (short-night vs. long-night) modulate the response to LPS.

Main Methods:

• Ewes were exposed to either short-night (SN) or long-night (LN) photoperiods and randomly assigned to control (saline) or LPS-treated groups.
• Blood samples were collected to measure hormone concentrations (melatonin, cortisol) via radioimmunoassay.
• Pineal gland tissue was analyzed for serotonin content (HPLC) and the expression of melatonin pathway enzymes (real-time PCR, Western Blot).

Main Results:

• LPS administration reduced circulating melatonin levels in LN ewes during the first hour and in SN ewes during the third hour post-treatment.
• Inflammation more significantly suppressed melatonin biosynthesis in SN ewes, which also showed lower cortisol levels.
• In SN ewes, LPS decreased pineal serotonin content and the expression of key enzymes like tryptophan hydroxylase and arylalkylamine-N-acetyltransferase.

Conclusions:

• Peripheral inflammation induced by LPS demonstrably reduces melatonin secretion in ewes.
• The suppressive effect of inflammation on melatonin production is significantly influenced by the prevailing photoperiodic conditions.
• The pineal gland's activity may be disrupted by circulating LPS and inflammatory cytokines, as indicated by receptor expression in the gland.