Activation of Inflammatory Networks in the Lungs Caused by Chronic Cold Stress Is Moderately Attenuated by Glucose Supplementation

Abstract

Mammals that live in cold climates endure months of exposure to low temperature in the winter. The incidence of respiratory diseases has increased. The goal of this study was to investigate the effects of chronic cold stress on lung inflammatory networks, apoptosis, and mitochondrial function via Yorkshire pig models, as well as the ameliorative effect of glucose as energy supplements. Here, two trials were conducted (chronic cold stress and glucose supplementation). The results showed that chronic cold stress induced obvious inflammatory cell infiltration in the lungs and damaged the lung tissue structure. Compared with the Y-Con group, the expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), high mobility group box 1 (HMGB1), nucleotide-binding domain, and leucine-rich repeat protein 3 (NLRP3), IL-1β, IL-2, IL-6, and IFN-γ in the lungs of the Y-CS group was enhanced by chronic cold stress (p < 0.05). Moreover, chronic cold stress promoted the expression of the Bax and Mfn2 in lungs of Y-CS group (p < 0.05). Interestingly, dietary glucose supplementation significantly reduced inflammatory cell infiltration in the lungs. Moreover, glucose supplementation inhibited the expression of TLR4, MyD88, HMGB1, NLRP3, IL-1β, IL-2, IL-6, IFN-γ, and Bax during chronic cold stress. In conclusion, chronic cold stress promoted inflammatory networks, apoptosis, and mitochondrial fusion in the lungs. Dietary glucose supplementation inhibited the inflammatory network during chronic cold stress.

Dietary full-fat rice bran prevents the risk of heart ferroptosis and imbalance of energy metabolism induced by prolonged cold stimulation

“…54,55 Our previous study showed that prolonged cold stimulation induces inflammation by activating the TLR4/NLRP3 signaling pathway in the small intestinal mucosa and lungs. 18,19 In the present study, there was no effect on the protein expression of MyD88 even though its mRNA expression was enhanced during prolonged cold stimulation. Nevertheless, the protein levels of NLRP3 and mature-Il-1β were promoted.…”

“…Numerous studies have demonstrated that extended exposure to cold in animals causes an inflammatory reaction and tissue damage. 19 Our results showed that prolonged cold stimulation promoted the IL-6, IFN-γ, and TNF-α mRNA expression in the heart. ANP, BNP, and MYH7 are markers of cardiac hypertrophy, which are commonly upregulated with the onset of cardiac hypertrophy.…”

“…Organs and systems may sustain varying degrees of injury when temperatures drop below the tolerance of humans. 18,19 The heart primarily powers the circulation of blood in the body. Previous studies have shown that shortterm cold stimulation increases heart output and blood flow, helping the body fight the cold.…”

Intermittent mild cold stimulation alleviates cold stress-induced pulmonary fibrosis by inhibiting the TGF-β1/Smad signaling pathway in broilers

“…Cold stress is a common stressor for livestock and poultry living in the northern regions during winter ( Olfati et al, 2018 ; Teng et al, 2022 ). Numerous studies have reported that cold stress reduces body weight and production performance in chickens and causes oxidative damage ( Olfati et al, 2018 ; Wei et al, 2018 ; Su et al, 2020 ).…”

“…Cold stress is an environmental factor that has evident impact on the welfare and health of humans, livestock, and poultry living in the northern regions of the globe ( Wei et al, 2018 ; Teng et al, 2022 ). Numerous studies have reported a significant reduction in production performance and body weight gain of chickens under cold stress ( Zhang et al, 2016 ; Olfati et al, 2018 ).…”