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Neuroinflammatory reactions in sickness behavior induced by bacterial infection: Protective effect of minocycline
Hanaa A Mansour1, Wedad A Hassan1, Gehan S Georgy1
1Department of Pharmacology, National Organization for Drug Control and Research, NODCAR, Giza, Egypt.
Abstract:
The neurological changes elicited by bacterial infection are called sickness behavior. Minocycline (MIN) is neuroprotective with a remarkable brain tissue penetration. MIN was orally administered at a dose 90 mg/kg for 3 days, whereas Escherichia coli was given as a single intraperitoneal injection (0.2 mL of 24 h growth) on the third day. After 24 h of bacterial infection, behavioral tests namely open field and forced swimming were carried out, then animals were decapitated. Rats infected with E. coli displayed reduced struggling time in forced swimming test, as well as, exploration and locomotion in open field test with reduction in neurotransmitters (norepinephrine, dopamine, and serotonin) versus elevation in the inflammatory (tumor necrosis factor-alpha, interferon-gamma) and oxidative stress (thiobarbituric acid reactive substance, reduced glutathione) biomarkers. Inflammatory infiltrates of nuclear cells were observed in brains of infected rats. MIN administration prevented the deleterious effects of E. coli infection, thus protects against sickness behavior possibly via defending from neuroinflammation.
Insights
Minocycline (MIN) protects against bacterial infection-induced sickness behavior by reducing neuroinflammation. This antibiotic treatment reversed behavioral deficits and normalized neurotransmitter levels in rats challenged with Escherichia coli.
Area of Science:
- Neuroscience
- Pharmacology
- Infectious Diseases
Background:
- Bacterial infections can trigger neurological changes known as sickness behavior.
- Minocycline (MIN) is a neuroprotective antibiotic with excellent brain penetration.
Purpose of the Study:
- To investigate the neuroprotective effects of Minocycline against Escherichia coli-induced sickness behavior in rats.
- To evaluate Minocycline's impact on neurotransmitters, inflammation, and oxidative stress markers in the brain.
Main Methods:
- Rats were administered Minocycline (90 mg/kg orally) for 3 days.
- Escherichia coli infection was induced via intraperitoneal injection on day 3.
- Behavioral tests (open field, forced swimming), neurotransmitter analysis, and biomarker assessment were performed 24 hours post-infection.
Main Results:
- E. coli infection caused reduced struggling time, impaired locomotion/exploration, altered neurotransmitter levels, and increased inflammatory/oxidative stress biomarkers.
- Histological examination revealed inflammatory infiltrates in the brains of infected rats.
- Minocycline administration attenuated these negative effects, protecting against sickness behavior.
Conclusions:
- Minocycline effectively counteracts the neurobiological and behavioral consequences of bacterial infection.
- The neuroprotective mechanism of Minocycline may involve the mitigation of neuroinflammation and oxidative stress.
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