Table 1.

The effects of heat stress-induced neuronal/humoral factors on intestinal physiology and gut microbiota.

Factors	Effects	Species	References
HSF, HSP, and TLR	Induced oxidative stress and intestinal barrier breakdown, initiated inflammatory signaling	Chicken	Varasteh et al., 2015
Proinflammatory cytokines (e.g., IL-1β, IL-2, IL-6, and TNF-α)	Damaged tight junction and gut epithelial integrity, activated HPA axis, enhanced successful transmission of pathogens	Chicken	Al-Sadi et al., 2010; Deng et al., 2012; Alhenaky et al., 2017; Jiang et al., 2021
Corticosterone	Altered HPA axis, increased macrophage oxidative burst and decreased numbers of macrophage undergoing phagocytosis, depressed immune response, induced intestinal lesions, altered gut microbial communities	Chicken	Deng et al., 2012; Quinteiro-Filho et al., 2012b; Beckford et al., 2020; Zaytsoff et al., 2020
Monoamines (e.g., 5-HT, NE, E, and DA)	Increased corticosterone and inflammatory cytokines	Chicken, rat	Johnson et al., 2005; Bahry et al., 2017
Appetite-related neuropeptides (e.g., CCK, ghrelin, CRF, and NPY)	Reduced food intake, activated HPA axis and stress response, impaired intestinal structure	Chicken	Lei et al., 2013; Bohler et al., 2020; Wang et al., 2021
Reactive oxygen and/or nitrogen species	Abnormal heat tolerance, injured intestinal barrier, invading pathogens, translocated endotoxins, increased inflammatory cytokines	Rat	Hall et al., 2001

5-HT, 5-hydroxytryptamine; CCK, cholecystokinin; CRF, corticotropin-releasing factor; DA, dopamine; E, epinephrine; HPA axis, hypothalamic-pituitary-adrenal axis; HSF, heat shock factor; HSP, heat shock protein; IL, interleukin; NE, norepinephrine; NPY, neuropeptide Y; TLR, toll-like receptor; and TNF-α, tumor necrosis factor-α.