Melatonin modulates allergic lung inflammation

Martins, Eivor; Oliveira, Ana Paula Ligeiro de; Araújo, A.M. Fialho de; Lima, Wothan Tavares de; Cipolla‐Neto, José; Rosa, Louis Fernando B. P. Costa

doi:10.1034/j.1600-079x.2001.310412.x

Cited by 45 publications

(29 citation statements)

References 32 publications

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“…In other studies, pineal removal further elucidated the effect of melatonin on the immune system. Pineal excision leads to a partial immune function deficiency, such as decreased IL-2 production (Delgobbo et al 1989), impaired colony forming units of granulocytes and macrophages from rat bone marrow cell cultures (Haldar et al 1992), and changed allergic lung inflammation (Martins et al 2001). All previous studies confirmed the considerable role of melatonin in immune system stabilization.…”

Section: Introductionsupporting

confidence: 63%

Exogenous melatonin inhibits neutrophil migration through suppression of ERK activation

Ren¹,

Sun²,

Li³

et al. 2015

Journal of Endocrinology

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Neutrophil migration to inflammatory sites is the fundamental process of innate immunity among organisms against pathogen invasion. As a major sleep adjusting hormone, melatonin has also been proved to be involved in various inflammatory events. This study aimed to evaluate the impact of exogenous melatonin on neutrophil migration to the injury site in live zebrafish and further investigate whether ERK signaling is involved in this process. Using the tail fin transection model, the fluorescently labeled neutrophil was in vivo visualized in transgenic Tg(lyz:EGFP), Tg(lyz:DsRed) zebrafish. We found that exogenous melatonin administration dramatically inhibited the injury-induced neutrophil migration in a dose-dependent and time-dependent manner. The inhibited effect of melatonin on neutrophil migration could be attenuated by melatonin receptor 1, 2, and 3 antagonists. The ERK phosphorylation level was significantly decreased post injury when treated with melatonin. The blocking of ERK activation with inhibitor PD0325901 suppressed the number of migrated neutrophils in response to injury. However, the activation of ERK with the epidermal growth factor could impair the inhibited effect of melatonin on neutrophil migration. We also detected that PD0325901 significantly suppressed the in vivo neutrophils transmigrating over the vessel endothelial cell using the transgenic Tg(flk:EGFP);(lyz:DsRed) line labeled as both vessel and neutrophil. Taking all of these data together, the results indicated that exogenous melatonin had an anti-migratory effect on neutrophils by blocking the ERK phosphorylation signal, and it led to the subsequent adhesion molecule expression. Thus, the crossing of the vessel endothelial cells of neutrophils became difficult.

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Section: Introductionsupporting

confidence: 63%

Exogenous melatonin inhibits neutrophil migration through suppression of ERK activation

Ren¹,

Sun²,

Li³

et al. 2015

Journal of Endocrinology

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“…It was described that the removal of the pineal gland causes partial (and transient) impairment of immune response in rats [44,53,54]; moreover, NK activity and IL-2 production were described to be reduced in rats after pinealectomy [44].…”

Section: Neuro-endocrine Melatonin: Systemic Effects Of Pineal Melatomentioning

confidence: 99%

“…For example, Martins et al, in an experimental model of allergic airway inflammation, showed that melatonin administration to pinealectomized rats restores the ability of cells to migrate from the bone marrow to the broncho-alveolar fluid, which was prevented after pineal gland removal, implying that neuro-endocrine melatonin is important in the control of cell recruitment from the bone marrow and the migration of those cells to the lung [54] As the melatonin-dependent effects of pinealectomy on the immune response appear to be partial, this further indicates that other compartments can overcome or contribute to immunomodulatory effects triggered by melatonin. M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 by specifically inhibiting melatonin signaling by the MT1/MT2 antagonist luzindole [55].…”

Section: Neuro-endocrine Melatonin: Systemic Effects Of Pineal Melatomentioning

confidence: 99%

Melatonin: A pleiotropic molecule regulating inflammation

Radogna

Diederich

Ghibelli

2010

Biochemical Pharmacology

308

247

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Melatonin is a neurohormone produced by the pineal gland that regulates sleep and circadian functions. Melatonin also regulates inflammatory and immune processes acting as both an activator and inhibitor of these responses. Melatonin demonstrates endocrine, but also paracrine and autocrine effects in the leukocyte compartment: on one side, leukocytes respond to melatonin in a circadian fashion; on the other side, leukocytes are able to synthesize melatonin by themselves.With its endocrine and paracrine effects, melatonin differentially modulates pro-inflammatory enzymes, controls production of inflammatory mediators such as cytokines and leukotrienes and regulates the lifespan of leukocytes by interfering with apoptotic processes. Moreover, its potent anti-oxidant ability allows scavenging of oxidative stress in the inflamed tissues. The interesting timing of pro-and anti-inflammatory effects, such as those affecting lipoxygenase activity, suggests that melatonin might promote early phases of inflammation on one hand and contribute to its attenuation on the other hand, in order to avoid complications of chronic inflammation. This review aims at giving a comprehensive overview of the various inflammatory pathways regulated by this pleiotropic hormone.

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“…Melatonin has been reported to have a beneficial effect on inflammatory lung diseases (17). Herein, we found a protective effect of melatonin by measuring the levels of pro-inflammatory cytokines and leukocyte accumulation in the serum and BAL fluid of mice with lung inflammation induced by LPS and SD.…”

Section: Discussionmentioning

confidence: 79%

Melatonin improves inflammatory cytokine profiles in lung inflammation associated with sleep deprivation

et al. 2012

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Abstract. Sleep disturbance has become an endemic behavior in modern countries, and its prevalence has also increased. Even a subtle sleep deficiency is related to health problems. Particularly, patients with pulmonary disease often complain of insomnia. We recently showed that sleep deprivation (SD) exacerbates existing acute lung inflammation, and that melatonin treatment attenuates it via anti-apoptotic and anti-oxidant action. In order to reinforce our previous report, the present study was designed to evaluate pro-inflammatory mediators in acute lung inflammation in SD mice. In addition, we investigated the infiltration of inflammatory cells into the lungs. Twenty-five ICR mice were divided into 5 groups (n=5/ group): control, SD, lipopolysaccharide (LPS), LPS + SD and LPS + SD + melatonin. The SD mice were deprived of sleep for 96 h in a multiplatform water bath. LPS (5 mg/kg) and melatonin (5 mg/kg) were administered on day 2. The mice were sacrificed on day 3, and serum and bronchoalveolar lavage (BAL) fluid were collected. The serum levels of inflammatory cytokines were increased in the LPS + SD group. Interleukin-6, tumor necrosis factor-α and interferon-γ levels were also increased in BAL fluid in the LPS + SD group. Melatonin reduced inflammatory mediators in the serum and BAL fluid. The accumulation of leukocytes in the LPS and LPS + SD mice was elevated, however, melatonin inhibited the recruitment of inflammatory cells (p<0.05). Lymphocytes in the BAL fluid of the LPS + SD group were increased, and macrophage levels were decreased; however, the increment was attenuated by melatonin administration (p<0.05). In conclusion, this study indicates that melatonin has a protective effect against lung inflammation associated with SD.

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Melatonin modulates allergic lung inflammation

Cited by 45 publications

References 32 publications

Exogenous melatonin inhibits neutrophil migration through suppression of ERK activation

Exogenous melatonin inhibits neutrophil migration through suppression of ERK activation

Melatonin: A pleiotropic molecule regulating inflammation

Melatonin improves inflammatory cytokine profiles in lung inflammation associated with sleep deprivation

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