Table 1.

Key findings related to the role of selenium in animal models of bacterial infections.

Study	Year	Model	Pathogen	Selenium*	Dose & Route**	Major Findings
Gao [116]	2016	Mouse	S. aureus	NaSe	0.03, 0.13, 1.5mg/kg diet	Deficiency lead to higher levels of proinflammatory cytokines, MPO activity, TLR2 signaling and NF-κB activation.
Smith [117]	2011	Mouse	C. rodentium	NaSe	0 or 0.2μg/g diet	Deficiency lead to increased cytokine levels, pathology and colonic hyperplasia. Maintenance of diet for 20 weeks verses 5 weeks exacerbated phenotype.
Smith [90]	2011	Mouse	C. rodentium	NaSe (Vit E)	0 or 0.2μg/g diet	Vitamin E and Se deficiency lead to increased bacterial burden reduced response and increased pathology.
Wang [99]	2009	Mouse	L. monocytogenes	Se	0.005 or 0.2mg/kg diet	Deficiency lead to increased bacterial burden, less infiltrating immune cells in the spleen and NK cells had lower activity.
Berg [118]	2005	Mouse	E. coli LPS	NaSe	0.05, 0.15, 2g/kg diet	Deficiency was marked by reduced levels of GPX in a dose dependent manner.
Altimira [119]	2000	Mouse	L. monocytogenes	Se	350 or <8μg/g diet	Deficiency leads to greater damage in CNS tissue.
Liu [88]	2016	Rat	S. aureus	MCS/MSA	1.5mg/kg Se i.p.	Deficiency leads to increased TRL-2 activation increasing caspase cleavage and apoptosis.
Kim [120]	2012	Rat	E. coli	Se	12μg/g water	Se with ciprofloxacin decreased bacterial burden.
Boyne [121]	1986	Rat	S. typhimurium S. aureus	Se	0.01 or 0.1 mg/kg	Deficiency had no effect on response to infection.
Sjunnesson [122]	2001	Guinea Pig	H. pylori	Se (Vit: A,C, E)	0.15 or 1 mg/kg diet	Dietary antioxidant levels increased with supplementation this protected against type-B gastritis. Data suggest there may be a correlation between bacterial load and gastric scores.

^*Forms of Se: sodium selenite (NaSe), unknown or labeled as selenium (Se), selenium nanoparticles (SeNp), methylselenocysteine (MCS), methylseleninic acid (MSA)

^**Intraperitoneal injection (i.p.)