Exploration of Acute Phase Proteins and Inflammatory Cytokines in Early Stage Diagnosis of Acute Mountain Sickness

Wang, Chi; Jiang, Hui; Duan, Jinyan; Chen, Jingwen; Wang, Qi; Liu, Xiaoting; Wang, Chengbin

doi:10.1089/ham.2017.0126

Cited by 38 publications

(40 citation statements)

References 43 publications

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“…Here, IL-1β mRNA expression was increased and this was associated with an increased LLS. Thus, one might emphasize that alteration in serum cytokine concentrations under hypoxia might be associated with clinical symptoms of AMS: this is in accordance with previous studies showing that IL-1β, IL-6, and TNF-α were increased in AMS patients, or that an inhibition of anti-inflammatory IL-10 was associated with AMS in a genome wide study [31,37,38]. In contrast, other studies did not find an association between circulating cytokines like IL-3, IL-6, or IL-10, exercise and AMS [38][39][40].…”

Section: Discussionsupporting

confidence: 89%

“…It is known that both exercise and hypoxia can alter mRNA expression and protein release of pro-and anti-inflammatory cytokines, like interleukin-1β (IL-1β), IL-6, or IL-10, activate lymphocytes, alter chemokine receptors, or induce further signaling pathways of the hypoxic inflammatory response [27][28][29]. Especially, in high altitude cerebral edema (HACE) proinflammatory cytokines like IL-1β, IL-6, or vascular endothelial growth factor A (VEGF-A) are believed to play an important role [30,31]. Apart from pro-and anti-inflammatory cytokines, the role of chemokines is of particular importance, as chemokine expression and its ligands are crucial for immune cell migration, e.g., in neuroinflammatory processes, and could therefore also be of interest with respect to hypobaric hypoxia-induced AMS and high altitude cerebral edema (HACE) [32][33][34].…”

Section: Introductionmentioning

confidence: 99%

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Hypoxic-Inflammatory Responses under Acute Hypoxia: In Vitro Experiments and Prospective Observational Expedition Trial

Kämmerer

Faihs

Hulde

et al. 2020

IJMS

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Induction of hypoxia-inducible-factor-1α (HIF-1α) pathway and HIF-target genes allow adaptation to hypoxia and are associated with reduced incidence of acute mountain sickness (AMS). Little is known about HIF-pathways in conjunction with inflammation or exercise stimuli under acute hypobaric hypoxia in non-acclimatized individuals. We therefore tested the hypotheses that (1) both hypoxic and inflammatory stimuli induce hypoxic-inflammatory signaling pathways in vitro, (2) similar results are seen in vivo under hypobaric hypoxia, and (3) induction of HIF-dependent genes is associated with AMS in 11 volunteers. In vitro, peripheral blood mononuclear cells (PBMCs) were incubated under hypoxic (10%/5% O2) or inflammatory (CD3/CD28) conditions. In vivo, Interleukin 1β (IL-1β), C-X-C Chemokine receptor type 4 (CXCR-4), and C-C Chemokine receptor type 2 (CCR-2) mRNA expression, cytokines and receptors were analyzed under normoxia (520 m above sea level (a.s.l.)), hypobaric hypoxia (3883 m a.s.l.) before/after exercise, and after 24 h under hypobaric hypoxia. In vitro, isolated hypoxic (p = 0.004) or inflammatory (p = 0.006) stimuli induced IL-1β mRNA expression. CCR-2 mRNA expression increased under hypoxia (p = 0.005); CXCR-4 mRNA expression remained unchanged. In vivo, cytokines, receptors, and IL-1β, CCR-2 and CXCR-4 mRNA expression increased under hypobaric hypoxia after 24 h (all p ≤ 0.05). Of note, proinflammatory IL-1β and CXCR-4 mRNA expression changes were associated with symptoms of AMS. Thus, hypoxic-inflammatory pathways are differentially regulated, as combined hypoxic and exercise stimulus was stronger in vivo than isolated hypoxic or inflammatory stimulation in vitro.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Hypoxic-Inflammatory Responses under Acute Hypoxia: In Vitro Experiments and Prospective Observational Expedition Trial

Kämmerer

Faihs

Hulde

et al. 2020

IJMS

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“…interleukin 1β (IL-1β), and interleukin 6 (IL-6) (Bouchama et al 1993) and lower concentrations of interleukin 10 (IL-10) (Welc et al 2013). Of note, individuals that develop acute mountain sickness (AMS), which is a common illness during travel to high altitude (Burns et al 2018), also exhibit elevated circulating concentrations of inflammatory cytokines (TNF-α, IL-1β, and IL-6) (Wang et al 2018) and lower levels of anti-inflammatory cytokines (IL-10 and IL-1Ra) (Liu et al 2017). In contrast, higher levels of anti-inflammatory cytokines have been shown to afford protection against AMS (Julian et al 2011).…”

Section: Introductionmentioning

confidence: 99%

Prolonged treadmill running in normobaric hypoxia causes gastrointestinal barrier permeability and elevates circulating levels of pro- and anti-inflammatory cytokines

Hill

Gillum

Lee

et al. 2020

Appl. Physiol. Nutr. Metab.

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This study examined the impact of treadmill running in normobaric hypoxia on gastrointestinal barrier permeability and the systemic inflammatory response. Ten recreationally active participants completed two 1-h bouts of matched-workload treadmill exercise (65% normoxic maximal oxygen consumption) in counterbalanced order. One bout was performed in normoxia (NORM: fraction of inspired oxygen (FIO2) = 20.9%) and the other in normobaric hypoxia (HYP: FIO2 = 13.5%). Minute ventilation, respiratory rate (RR), tidal volume (VT), oxygen consumption, carbon dioxide production, respiratory exchange ratio (RER), and heart rate (HR) were measured with a metabolic cart. Peripheral oxygen saturation (SpO2) was measured with pulse oximetry. Absolute tissue saturation (StO2) was measured with near-infrared spectroscopy. Fatty acid-binding protein (I-FABP) and circulating cytokine concentrations (interleukin (IL)-1Ra, IL-6, IL-10) were assayed from plasma samples that were collected pre-exercise, postexercise, 1 h-postexercise, and 4 h-postexercise. Data were analyzed with 2-way (condition × time) repeated-measures ANOVAs. Newman–Keuls post hoc tests were run where appropriate (p < 0.05). As compared with NORM, 1 h of treadmill exercise in HYP caused greater (p < 0.05) changes in minute ventilation (+30%), RR (+16%), VT (+10%), carbon dioxide production (+18%), RER (+16%), HR (+4%), SpO2 (–16%), and StO2 (–10%). Gut barrier permeability and circulating cytokine concentrations were also greater (p < 0.05) following HYP exercise, where I-FABP was shown increased at postexercise (+68%) and IL-1Ra at 1 h-postexercise (+266%). I-FABP and IL-1Ra did not change (p > 0.05) following NORM exercise. IL-6 and IL-10 increased with exercise in both study conditions but were increased more (p < 0.05) following HYP at postexercise (+705% and +127%, respectively) and 1 h-postexercise (+400% and +128%, respectively). Novelty Normobaric hypoxia caused significant desaturation and increased most cardiopulmonary responses by 10%–30%. Significant gut barrier permeability and increased pro- and anti-inflammatory cytokine concentrations could promote an “open window” in the hours following HYP exercise.

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“…AMS is a predominant neurological disorder, and it is controversial whether minor impairments of gas exchange contribute to this disease (Cremona et al, 2002;Senn et al, 2006;Dehnert et al, 2010;Berger et al, 2017;Lipman et al, 2017). The significance of inflammation in AMS is in general unclear, as previous studies found either no ( Johnson et al, 1988;Kleger et al, 1996;Swenson et al, 1997;Julian et al, 2011) or only a moderate (Hartmann et al, 2000;Boos et al, 2016;Lundeberg et al, 2018;Wang et al, 2018) increase (of about 1.5-to 3.5-fold) in proinflammatory cytokines in subjects with AMS. Even if some mild inflammation is part of the pathophysiology of AMS, it does not induce organ damage and its significance in the disease's pathogenesis is far smaller than in COVID-19.…”

Section: Role Of Inflammationmentioning

confidence: 99%

No Relevant Analogy Between COVID-19 and Acute Mountain Sickness

Berger

Hackett

Bärtsch

2020

High Altitude Medicine & Biology

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No relevant analogy between COVID-19 and acute mountain sickness. High Alt Med Biol 00:000-000, 2020.-Clinicians and scientists have suggested therapies for coronavirus disease-19 (COVID-19) that are known to be effective for other medical conditions. A recent publication suggests that pathophysiological mechanisms underlying acute mountain sickness (a syndrome of nonspecific neurological symptoms typically experienced by nonacclimatized individuals at altitudes >2500 m) may overlap with the mechanisms causing COVID-19. In this short review, we briefly evaluate this mistaken analogy and demonstrate that this concept is not supported by scientific evidence.

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Exploration of Acute Phase Proteins and Inflammatory Cytokines in Early Stage Diagnosis of Acute Mountain Sickness

Cited by 38 publications

References 43 publications

Hypoxic-Inflammatory Responses under Acute Hypoxia: In Vitro Experiments and Prospective Observational Expedition Trial

Hypoxic-Inflammatory Responses under Acute Hypoxia: In Vitro Experiments and Prospective Observational Expedition Trial

Prolonged treadmill running in normobaric hypoxia causes gastrointestinal barrier permeability and elevates circulating levels of pro- and anti-inflammatory cytokines

No Relevant Analogy Between COVID-19 and Acute Mountain Sickness

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