Gut health, stress, and immunity in neonatal dairy calves: the host side of host-pathogen interactions

Table 1 The impact of perinatal stressors or conditions on indicators of intestinal development or maturation

Stressor or effect^a	Species or model^b	Effect on intestinal development^c	Age measured, d	Reference
IUGR	Sheep	↓ Intestinal mass and length ↓ Crypt depth and mucosal size	90 and 140 d of gestation	[23, 24]
Nutrient restriction	Cow	↓ Villus and crypt density ↑ Duodenal upregulation of SLC5A1, CD36, and CCK	135 d postnatal	[25]
IUGR	Sheep	↓ Villus height and width	90 d of gestation	[23]
Nutrient restriction	Sheep	↓ Jejunum vascularity and GUCY1B3	135 d of gestation	[26]
Overnutrition	Sheep	↑ Jejunal hyperplasia and vascularity	20 and 180 d postnatal	[27, 28]
Heat stress	Cow	↓ Passive immune transfer due to reduced intestinal surface area	1 and 2 d postnatal	[29]
Negative DCAD diet	Cow	↓ Colostrum IgG absorption	1–2 d postnatal	[32]
Negative DCAD diet	Cow	↔ Colostrum IgG absorption	1 d postnatal	[21]
Injected cortisol	Rabbit	↑ Brush border enzymes and Na⁺/K⁺ ATPase	10–12 d postnatal	[33]
Cortisol	H4 cells	↑ Gene related to cell polarity, tight junction formation, and interactions with extracellular matrices	–	[34]
Cortisol	H4 cells	↓ Attenuates proinflammatory insults	–	[35]
miRNAs	Mouse and IPEC-J2 cells	↑ Villus height and crypt depth	–	[36]

^aIUGR = Intrauterine growth retardation; DCAD = dietary cation-anion difference; miRNAs = microRNAs (~ 18–25 nucleotides)
^bH4 cells = human fetal small intestinal epithelial cell line; IPEC-J2 = porcine small intestinal epithelial cell line
^c↑ = increase; ↓ = decrease; ↔ = no effect

ISSN: 2049-1891