Multiple factors, such as environment, nutritional status, and disease, induce stress in animals during livestock production. It has been shown that

Endocannabinoid signaling is terminated by enzymatic hydrolysis, a process that, for 2-Arachidonoylglycerol (2-AG), is mediated by monoacylglycerol lipase (MAGL). The piperidine carbamate, 4-​nitrophenyl- ​4-​(dibenzo[d] [1,3]dioxol-​5-​yl (hydroxy) methyl) piperidine- 1-​carboxylate (JZL184), is a drug that inhibits MAGL and presents high potency and selectivity. Thus, JZL184 increases the levels of 2-AG, an endocannabinoid that acts on the CB₁ and CB₂ cannabinoid receptors. Here, we investigated the effects of MAGL inhibition, with a single dose (16 mg/kg, intraperitoneally (i.p.)) of JZL184, in a murine model of lipopolysaccharide (LPS) -induced acute lung injury (ALI) 6, 24 and 48 hours after the inflammatory insult. Treatment with JZL184 decreased the leukocyte migration into the lungs as well as the vascular permeability measured through the bronchoalveolar lavage fluid (BAL) and histological analysis. JZL184 also reduced the cytokine and chemokine levels in the BAL and adhesion molecule expression in the blood and BAL. The CB₁ and CB₂ receptors were considered involved in the anti-inflammatory effects of JZL184 because the AM281 selective CB₁ receptor antagonist (1-(2,4-dichlorophenyl)-5-(4-iodophenyl)-4-methyl-N-4-morpholinyl-1H-pyrazole-3-carboxamide) and the AM630 selective CB₂ receptor antagonist ([6-​iodo-​2-​methyl-​1-​[2-​(4-​morpholinyl)ethyl]-​1H-​indol-​3-​yl](4-​methoxyphenyl)-​methanone) blocked the anti-inflammatory effects previously described for JZL184. It was concluded that MAGL inhibition, and consequently the increase in 2-AG levels, produced anti-inflammatory effects in a murine model of LPS-induced ALI, a finding that was considered a consequence of the activation of the CB₁ and CB₂ receptors.

The intensification of poultry production has favoured the occurrence of stressful conditions such as infections, decreased feed intake, reduced feed conversion and carcass condemnation are some of the consequences of stress in birds. This stress is a consequence of the neuroendocrine-immune interplay. Neuroimmunomodulation is the scientific study of the bidirectional relation of the immune and nervous systems, i.e., physiological effects in response to exposure of animals to stressful conditions. Stress is responsible for activating the hypothalamic-pituitary-adrenal axis, which results in the production and release of corticosterone and catecholamines. Furthermore, recent studies have shown that the brain-gut-microbiota axis is responsible for the maturation and maintenance of the balance of the immune and nervous systems, which ensures improvement in the productive system. This review presents and discusses information concerning neuroimmunomodulation in birds with an emphasis on the involvement of heat stress.

Stressful conditions are predisposing factors for disease development. Heat stress is one of the most important stressors in poultry production. The