Table 2.

The immune and inflammatory response generates the sickness syndrome, i.e., the sickness behaviour, the pain and fatigue response and the acute‐phase reaction. The classic stress syndrome is mostly antagonistic to the sickness syndrome (Modified with permission from Annals of the New York Academy of Sciences ⁸ )

	Sickness syndrome	Classic stress syndrome
Sickness behaviourPain and fatigue response Acute‐phase reaction	Anorexia/nausea	Anorexia/stimulation of appetite*
	Fatigue and/or depressed affect	Motivation/stimulated affect
	Somnolence	Arousal
	Hyperalgesia ± headache	Analgesia
	Elevated temperature/fever	Pyretic/antipyretic*
	Increased metabolic rate	Increased metabolic rate/return to normal*
	Acute‐phase reaction +++++	Acute‐phase reaction +
Cellular effectors	Immune and immune‐related cells, Neurones, endocrine cells	Immune and immune‐related cells
		Neurones, endocrine cells
Molecular effectors	Inflammatory cytokines/mediators, immune CRH	CRH, AVP, glucocorticoids, catecholamines, immune
		CRH, acetylcholine
	Transcription factors: GR, NF‐κB, CREB, AP1, STATs	Transcription factors: GR, NF‐κB, CREB, AP1, STATs

^* Initial stimulation via CRH and catecholamines, then inhibition by glucocorticoids.

AP1, activating protein 1; AVP, arginine‐vasopressin; CREB, cAMP response element‐binding protein; CRH, corticotropin‐releasing hormone; GR, glucocorticoid receptor; NF‐κB, nuclear factor kappa B; STAT, signal transducer and activator of transcription.

One to 5 +, degree of activation.