Evidence of “cross-stressor” - induced adaptive gastric cytoprotection

Glavin, Gary B.; Lockhart, Leslie K.; Rockman, Gary E.; Hall, Arleen M.; Kiernan, Kathleen M.

doi:10.1016/0024-3205(87)90519-4

Cited by 15 publications

(4 citation statements)

References 10 publications

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“…Whereas cold stimulation of lower 12°C resulted in tracheal mucosal injury, this may be caused by cold stress, indicating that birds could not adapt to this kind of low‐temperature stimulus. After ACS, the inflammatory injury in tracheal structure occurred for the birds in S1; however, the tracheal structure of S2 had no obvious lesions, similar to the results reported by Glavin et al () and Wallace et al (). This probably because such mild cold stimulation so that 3°C lower than the normal one reduced the sensitivity to tracheal mucosa injury, and it suggested that moderate cold stimulation could produce cold acclimation without causing morphological damage.…”

Section: Discussionsupporting

confidence: 88%

“…However, the adaptation mechanism produced by one kind of stressor to stimulate the body could protect the body from the damage of a variety of stressors. Glavin, Lockhart, Rockman, Hall, and Kiernan () pointed out that compared with the control group rats treated with water for 7 days, the gastric ulcer in the treatment group was significantly reduced when subjected to cold‐restraint stress after they adapted to the concentration of 20% alcohol for 7 days. Wallace, Track, and Cohen () also pointed out that compared with the rats in control group, the gastric mucosal injury of rats was significantly reduced when subjected to cold‐restraint stress after they adapted to chronic mild restraint stress for 2–10 days.…”

Section: Discussionmentioning

confidence: 99%

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Pre‐cold acclimation improves the immune function of trachea and resistance to cold stress in broilers

Wei

et al. 2018

Journal Cellular Physiology

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Acclimation can alleviate the damage caused by adverse environmental factors. To investigate the effects of cold stimulation on immunity in tracheal of broilers, 360 one-day-old chicks were raised at normal temperatures during 1-7 days. From 8 day, G1 (control) continued to be raised at normal temperatures, whereas G2 and G3 (treatment groups) were cold-stimulated at 3°C and 12°C below the temperature of G1, respectively. At 42 day, all the groups were subjected to a 24-hr acute cold stress, designated as S1, S2, and S3. Tracheal tissues were collected to detect gene levels of immunoglobulins, antimicrobial peptides, Hsps, and cytokines, and oxidative stressrelated indicators at 14 day, 42 day, and 43 day, and protein levels of Hsps and proinflammatory cytokines as well as morphology changes at 42 day and 43 day. The results showed that, compared with 42G1, tracheal structure of 42G2 was basically intact, and gene levels of immunoglobulins and antimicrobial peptides increased (p < 0.05), whereas tracheal structure of 42G3 was destroyed, with decreased levels of immunoglobulins (p < 0.05), and increased levels of Hsps and proinflammatory cytokines (p < 0.05). At 43 day, tracheal damage was visible and gene levels of immunoglobulins and antimicrobial peptides decreased in S1 (p < 0.05). Tracheal structure was relatively intact and gene levels of antimicrobial peptides increased in S2 (p < 0.05). Compared with S1 and S3, immune-related gene levels in S2 were higher, and Hsps and proinflammatory cytokines levels were lower. The results demonstrate that cold stimulation of lower 3°C from 8 to 42 day led to cold acclimation, which improved immunity of tracheal mucosa and resistance to cold stress in broilers.

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Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Pre‐cold acclimation improves the immune function of trachea and resistance to cold stress in broilers

Wei

et al. 2018

Journal Cellular Physiology

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“…23 The cross adaptation of mild irritants was further confirmed by showing that mild stress induced in rats by short restraint of animals in the cage, attenuated the formation of gastric lesions caused by severe stress as well as by the exposure of the mucosa to 40% ethanol. 25 The seven day pretreatment with mild stress or a low concentration of ethanol prevented the formation of mucosal lesions in rats subjected to strong restraint stress or absolute ethanol. 25 In another study, Uramoto et a126 have shown that the gastric mucosa of restraint loaded rats exerted a greater resistance to the damaging action of absolute ethanol.…”

Section: Discussionmentioning

confidence: 96%

“…25 The seven day pretreatment with mild stress or a low concentration of ethanol prevented the formation of mucosal lesions in rats subjected to strong restraint stress or absolute ethanol. 25 In another study, Uramoto et a126 have shown that the gastric mucosa of restraint loaded rats exerted a greater resistance to the damaging action of absolute ethanol. In their study, the protective effect of mild stress was significantly mitigated by vagotomy or indomethacin suggesting that vagal influences or endogenous prostaglandin, or both, could be involved in the mechanism of this cross adaptation.…”

Section: Discussionmentioning

confidence: 96%

Gastric adaptation to injury by repeated doses of aspirin strengthens mucosal defence against subsequent exposure to various strong irritants in rats.

Brzozowski

Konturek

et al. 1995

Gut

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Gastric adaptation to injury during repeated doses of acetyl salicylic acid (ASA) is a well documented finding but it is not known whether this adaptation affects the tolerance of the mucosa to other strong irritants. Gastric adaptation was induced by repeated daily doses of acidified ASA (100 mglkg in 1-5 ml of 0.2 N HCl) given intragastrically (series A rats). Control rats with an intact stomach were given daily intragastric vehicle only (1.5 ml of 0.2 N HCI) (series B). After full adaptation to ASA (5 days), rats were challenged again with acidified ASA or, for comparison, with strong irritants such as 100% ethanol, 200 mM acidified taurocholate, or 25% NaCl for 1 hour or with water immersion and restraint for 3.5 hours. The first dose of ASA produced numerous gastric lesions and deep histological necrosis accompanied by a fall in the gastric blood flow, negligible expression of epidermal growth factor (EGF) and transforming growth factor a (TGFa) or their receptors, and no evidence of mucosal proliferation. As adaptation to ASA developed, however, the areas of gastric lesions were reduced by more than 80% and there was a noticeable decrease in deep necrosis, a partial restoration of gastric blood flow, an approximately fourfold increase in EGF expression (but not in TGFIa) and its receptors, and an appreciable increase in mucosal celi proliferation compared with vehicle treated rats. Increases in the mucosal expression of EGF receptors and the luminal content of EGF were also found in ASA adapted animals. In ASA adapted rats subsequently challenged with 100% ethanol, 200 mM TC, 25% NaCI, or stress, the area of the gastric lesions and deep histological necrosis were appreciably reduced compared with values in vehicle treated rats. This increased mucosal tolerance to strong irritants was also accompanied by the return of the gastric blood flow towards control levels and further significant increases in the mucosal expression of EGF receptors and mucosal cell proliferation. Gastric adaptation to ASA enhances the mucosal resistance to injury by strong irritants probably as a result of the restoration of the gastric blood flow and increased celi proliferation that may result from increased mucosal expression of EGF and its receptors. (Gut 1995; 37: 749-757)

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