Reichenberg · Archives of general psychiatry 2001 · randomized double-blind crossover trial · n=20

Cytokine-associated emotional and cognitive disturbances in humans.

Cited 1380 times in the scientific literature.

Level 2 - randomized trial

Randomized double-blind crossover trial

PubMed 11343523 · doi:10.1001/archpsyc.58.5.445 · record verified 2026-08-29

What was done

In a double-blind crossover study, 20 healthy male volunteers completed psychological questionnaires and neuropsychological tests at 1, 3, and 9 hours after an intravenous injection of Salmonella abortus equi endotoxin (0.8 ng/kg) or saline across 2 experimental sessions. Blood samples were collected hourly to measure tumor necrosis factor alpha (TNF-alpha), soluble TNF receptors, interleukin (IL)-6, IL-1 receptor antagonist, and cortisol. Rectal temperature and heart rate were continuously monitored.

What was found

Endotoxin did not affect physical sickness symptoms, blood pressure, or heart rate, but caused a mild rectal temperature increase of 0.5 degrees C and elevated circulating levels of TNF-alpha, soluble TNF receptors, IL-6, IL-1 receptor antagonist, and cortisol. Following endotoxin injection, subjects exhibited a transient significant increase in anxiety (effect size [ES] = 0.55) and depressed mood (ES = 0.66), and a significant decrease in verbal and nonverbal memory functions (ES = 0.55 to 0.64). Cytokine secretion positively correlated with endotoxin-induced anxiety (r = 0.49 to r = 0.60), depressed mood (r = 0.40 to r = 0.75), and memory performance declines (r = 0.46 to r = 0.68).

Why it matters

This study provides experimental evidence in humans that systemic cytokine release induced by low-dose innate immune activation directly impairs emotional state and memory performance without causing overt physical illness.

Limits

The study was conducted in a small sample of only 20 individuals, all of whom were healthy males, limiting generalizability to females and clinical populations with chronic inflammation. The acute endotoxin challenge models transient immune activation rather than prolonged or chronic inflammatory states.

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