Corticosterone controls interleukin-1 beta expression and sickness behavior in the rat

Area of Science:

• Neuroendocrinology
• Immunology
• Behavioral Neuroscience

Background:

• Bacterial lipopolysaccharide (LPS) triggers inflammatory responses and sickness behavior in rodents.
• Corticosterone, a key glucocorticoid, plays a role in modulating immune and stress responses.
• Understanding the specific effects of corticosterone on LPS-induced sickness is crucial for inflammatory disease research.

Purpose of the Study:

• To investigate the impact of corticosterone on interleukin (IL)-1 beta synthesis, body temperature, and sickness behaviors (activity, feeding, drinking) in LPS-treated rats.
• To elucidate the role of corticosterone in regulating inflammatory responses and associated behavioral changes.

Main Methods:

• Utilized radiotelemetry for continuous monitoring of body temperature and locomotor activity.
• Employed automated recordings for feeding and drinking behaviors.
• Compared sham-operated, adrenalectomized, and corticosterone-treated rats following LPS or vehicle injection.

Main Results:

• Adrenalectomized rats exhibited elevated splenic IL-1 beta mRNA, reduced activity, and mild adipsia compared to controls.
• Corticosterone administration prior to LPS significantly reduced splenic IL-1 beta mRNA, fever, and anorexia.
• Corticosterone did not attenuate the LPS-induced decrease in locomotor activity.

Conclusions:

• Corticosterone is a key regulator of body temperature, sickness behavior, and IL-1 beta synthesis during inflammatory conditions.
• Different components of sickness behavior are independently regulated and differentially controlled by glucocorticoids.
• This study highlights the complex role of corticosterone in the integrated response to inflammation.