Table 1.

Surgical inflammation could be viewed as a high-degree stress response of the patient composed of three overlapping successive phenotypes

INFLAMMATORY PHENOTYPES IN SURGICAL INFLAMMATION
NEUROGENIC	IMMUNE	ENDOCRINE
- Stress sensation	- Bone marrow-related response	- Epiblast-derived pluripotent stem cells
- Inflammatory pain	- Hematopoietic stem cell activation	- Mesenchymal stem cell activation
- Fight-to-flight effect	- Signaling molecules:	- Fibrocytes
- Analgesia	* Chemokines	-Endothelial progenitor cells
- Hypothalamic-pituitary-adrenal cortical activation	* Toll-like receptors	- Signaling molecules:
	* Cytokines	* Chemokines and their receptors
- Sympatico-adrenal medullary activation	- Leukocyte activation	- Anabolic hormones
- Tachycardia	- Bacterial translocation	* Insulin
- Shock	- Enzymatic stress	* GH
- Ischemia-reperfusion	- Acute phase response	* IGF1
- Renin-angiotensin-aldosterone axis activation	- Coagulaton/Complement system activation	- CARS
		- Resolution
- Hydroelectrolytic alterations	- Coagulopathy	* Lipoxin
- Interstitial edema	- Dyslipidemia	* Resolvins
- Increased lymph flow	- SIRS/MODS	* Protectins
- Hypoxia	- Lymph node activation	- Angiogenesis/vasculogenesis
- Anaerobic acidosis	- Local stress response by leukocytes	- Blood capillaries
- Hypothermia	- Local cholesterol-derived hormones	- Specialezed epithelium
	- Hypercatabolism	- Energetic stress
	- Hypermetabolism	- Oxidative phosphorylation
		- Centralization of neuroendocrine functions
		- PTSD

CARS: Compensatory Anti-inflammatory Response Syndrome. SIRS/MODS: Systemic Inflammatory Response Syndrome/Multiple Organ Dysfunction Syndrome. PTSD: Post-Traumatic Stress Disorder.