High Altitude Increases Circulating Interleukin-6, Interleukin-1 Receptor Antagonist and C-Reactive Protein

Hartmann, Gunther; Tschöp, Matthias H.; Fischer, Rainald; Bidlingmaier, Christoph; Riepl, Rudolf L.; Tschöp, K.; Haŭtmann, Hŭbert; Endres, Stefan; Toepfer, Marcell

doi:10.1006/cyto.1999.0533

Cited by 400 publications

(331 citation statements)

References 33 publications

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“…Indeed hypoxia exposure whether, in vitro or in vivo, is associated with rise in inflammatory markers. However, in the previous studies, as also quoted in the article by the authors, the duration of hypoxia exposure varied from 16 to 72 h [2][3][4][5] On the contrary, in the present study duration of simulated hypoxia of 4500 m was only 30 min. It remains obscure that those changes seen in the chemokines are actually the result of hypoxia induced inflammation or otherwise.…”

Section: To the Editorcontrasting

confidence: 51%

Chemokines in High Altitude Pulmonary Edema

Bhattachar

Sikri

2016

Ind J Clin Biochem

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Section: To the Editorcontrasting

confidence: 51%

Chemokines in High Altitude Pulmonary Edema

Bhattachar

Sikri

2016

Ind J Clin Biochem

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“…IL6 secretion has been demonstrated to be facilitated by hypoxia in human umbilical vein and pulmonary endothelial cells, primary human pulmonary fibroblasts and vascular smooth muscle cells, and Kupffer cells as well as whole pulmonary artery organoid cultures (Yan et al, 1995(Yan et al, , 1997Tamm et al, 1998;Ziesche et al, 1996;Kotake-Nara et al, 2005;Sawa et al, 1998;Hartmann et al, 2000). Our previous studies found that the level of IL-6 was increased in pulmonary tissues of rats with hypoxia-induced pulmonary hypertension .…”

Section: Discussionmentioning

confidence: 95%

“…A number of studies have demonstrated that secretion of interleukins is facilitated by hypoxia (Yan et al, 1995(Yan et al, , 1997Tamm et al, 1998;Ziesche et al, 1996;Kotake-Nara et al, 2005;Sawa et al, 1998;Hartmann et al, 2000). Several studies have also indicated that Janus kinases (JAKs) and signal transducers and activators of transcription (STATs) are activated by interleukin 6 (IL6) in cardiomyocytes, macrophages, carcinoma cells and neurons and by hypoxia in pulmonary arterial smooth muscle cells, rat cardiomyocytes, retinal microvascular endothelial cells (Negoro et al, 2001;Mascareno et al, 2005;Wang et al, 2005;Dawn et al, 2004;Lee et al, 2006;Yamauchi et al, 2006;Terrell et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Sequential activation of JAKs, STATs and xanthine dehydrogenase/oxidase by hypoxia in lung microvascular endothelial cells

Wang

Pei

Jackson

et al. 2008

The International Journal of Biochemistry & Cell Biology

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Xanthine dehydrogenase/oxidase (XDH/XO) is associated with various pathological conditions related to the endothelial injury. However, the molecular mechanism underlying the activation of XDH/XO by hypoxia remains largely unknown. In this report, we determined whether the Janus kinases (JAKs) and signal transducers and activators of transcription (STATs) signaling pathway is involved in hypoxia-induced activation of XDH/XO in primary cultures of lung microvascular endothelial cells (LMVEC). We found that hypoxia significantly increased interleukin 6 (IL6) production in a time-dependent manner in LMVEC. Hypoxia also markedly augmented phosphorylation/activation of JAKs (JAK1, JAK2 and JAK3) and the JAK downstream effectors STATs (STAT3 and STAT5). Hypoxia-induced activation of STAT3 was blocked by IL6 antibodies, the JAK inhibitor AG490 and the suppressor of cytokine signaling 3 (SOCS3), implying that hypoxiapromoted IL6 secretion activates the JAK/STAT pathway in LMVEC. Phosphorylation and DNAbinding activity of STAT3 was also inhibited by the p38 MAPK inhibitor SB203580 and the phosphatidylinositol 3-kinase inhibitor LY294002, suggesting that multiple signaling pathways involved in STAT activation by hypoxia. Importantly, hypoxia promoted XDH/XO activation in LMVEC, which was markedly reversed by inhibiting the JAK/STAT pathway using IL6 antibodies, AG490 and SOCS3. These data demonstrated that JAKs, STATs and XDH/XO were sequentially activated by hypoxia. These data also provide the first evidence indicating that the JAK-STAT pathway is involved in hypoxia-mediated XDH/XO activation in LMVEC.

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“…Sabe-se que a hipoxemia da alta atitude e a privação do sono provocam aumento de IL6 e PCR em indivíduos normais (27). Portanto, nos pacientes com SAOS, a hipoxemia que ocorre repetidamente durante o sono, acompanhada da privação do sono, pode induzir a um estado sistêmico inflamatório, evidenciado pela elevação de PCR, amiloide A, IL-6 e TNF-α (9,28).…”

Section: Interações Entre Apnéia Do Sono E Resistência à Insulinaunclassified

Interações entre síndrome da apnéia obstrutiva do sono e resistência à insulina

Carneiro

Filho

Togeiro

et al. 2007

Arq Bras Endocrinol Metab

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RESUMOEstudos anteriores mostraram que pacientes com Apnéia Obstrutiva do Sono (AOS) apresentam maior risco para doenças cardiovasculares. Entretanto, permanece controverso se essa associação depende da obesidade ou se ocorre devido a alterações fisiológicas decorrentes da desordem do sono, como ativação do sistema nervoso simpático, da inflamação e desordens do eixo corticotrófico e somatotrófico, que predispõem a danos vasculares. Além disso, muitos fatores de risco para doenças cardiovasculares (DCV) estão fortemente associados ao distúrbio respiratório, entre eles hipertensão, obesidade, resistência à insulina e diabetes tipo 2 (DM2). Neste artigo, vamos discutir a interação entre resistência à insulina e AOS e os possíveis mecanismos fisiopatológicos que contribuem para suas co-morbidades. Previous studies have shown Obstructive Sleep Apnea (OSA) as a risk factor for development of cardiovascular and cerebrovascular disease. However, controversies remain as to whether these changes are consequences of the associated obesity or OSA itself results in endocrine and metabolic changes, including impairment of insulin sensitivity, growth hormone, secretion inflammatory cytokines alterations, activation of peripheral sympathetic activity, and hipothalamic-pituitary-adrenal (HPA) axis, that may predispose to vascular disease. Furthermore many cardiovascular risk factors, such as hypertension, obesity, insulin resistance and type 2 diabetes, are strongly associated with OSA. In this article, we will review the evidence and discuss possible mechanisms underlying these links and the pathophysiology of OSA morbidities.

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High Altitude Increases Circulating Interleukin-6, Interleukin-1 Receptor Antagonist and C-Reactive Protein

Cited by 400 publications

References 33 publications

Chemokines in High Altitude Pulmonary Edema

Chemokines in High Altitude Pulmonary Edema

Sequential activation of JAKs, STATs and xanthine dehydrogenase/oxidase by hypoxia in lung microvascular endothelial cells

Interações entre síndrome da apnéia obstrutiva do sono e resistência à insulina

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