Nicotine exposure alters<i>in vivo</i>human responses to endotoxin

Wittebole, Xavier; Hahm, Sae J.; Coyle, Susette M.; Kumar, Ashwini; Calvano, Steven E.; Lowry, Stephen F.

doi:10.1111/j.1365-2249.2006.03248.x

Cited by 77 publications

(61 citation statements)

References 35 publications

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“…*p # 0.05, Wilcoxon matched-pairs signed-rank test. cutaneous nicotine administration in humans increased IL-10 levels after LPS application (65). Very probably, monocytic cells (66), the a4 and b2 subunits of nicotinic acetylcholine receptor (67), and the increase of intracellular cyclic 39,59-adenosin-monophosphate levels (68) are involved in this nicotine effect.…”

Section: Discussionmentioning

confidence: 98%

Deficiency of IL-22 Contributes to a Chronic Inflammatory Disease: Pathogenetic Mechanisms in Acne Inversa

Wolk

Warszawska

Hoeflich

et al. 2011

The Journal of Immunology

227

283

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Overexpression of the T cell cytokine IL-22 is linked to the development of some chronic diseases, but little is known about IL-22 deficiency in humans. As demonstrated in this study, acne inversa (AI; also designated as Hidradenitis suppurativa) lesions show a relative deficiency of IL-22 and IL-20, but not of IL-17A, IL-26, IFN-γ, IL-24, or IL-1β. Moreover, AI lesions had reduced expression of membranous IL-22 and IL-20 receptors and increased expression of the natural IL-22 inhibitor, IL-22 binding protein. AI is a chronic inflammatory skin disease with prevalence up to 4% of the population and in which cutaneous bacterial persistence represents an important pathogenetic factor. Accordingly, we also found a relative deficiency of antimicrobial proteins (AMPs) in AI lesions and a positive correlation between lesional IL-22 and IL-20 versus AMP levels. IL-22, like its tissue cell downstream mediator IL-20, upregulated AMPs in reconstituted human epidermis and was critical for increased AMP levels under inflammatory conditions. The relative IL-22 deficiency in AI was not linked to lesional T cell numbers or Th22/Th1/Th17 subset markers and -inducing cytokines. However, IL-10 was highly expressed in AI lesions and correlated negatively with IL-22 expression. Moreover, IL-10 inhibited IL-22 but not IL-17 production in vitro. The IL-10 overexpression, in turn, was not associated with an elevated presence of regulatory T cells but with the enhanced presence of an IL-10–inducing cytokine. We conclude that IL-22 deficiency may contribute to the pathogenesis of certain chronic disorders as postulated in this paper for AI.

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Section: Discussionmentioning

confidence: 98%

Deficiency of IL-22 Contributes to a Chronic Inflammatory Disease: Pathogenetic Mechanisms in Acne Inversa

Wolk

Warszawska

Hoeflich

et al. 2011

The Journal of Immunology

227

283

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“…33 Factors that stimulate the release of ET-1 include endotoxins, interleukin-1, adrenaline, insulin, thrombin and angiotensin II. 34 There is much evidence showing that nicotine has strong endotoxic effect, 35,36 where nicotine stimulated ET-1 release, which induced endothelial injury. Both the reninangiotensin-aldosterone system (RAAS) and endothelin system are important endocrine modulation systems.…”

Section: Discussionmentioning

confidence: 99%

Deterioration of endothelial function and carotid intima-media thickness in Tibetan male adolescents exposed to second-hand smoke

Yang

Chen

et al. 2012

J Renin Angiotensin Aldosterone Syst

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Introduction: It has been commonly accepted that second-hand smoke (SHS) is associated with atherosclerosis and endothelial dysfunction. There is growing evidence that the changes might begin in childhood. Unfortunately, no study has focused on the early atherosclerosis of Tibetan adolescents exposed to SHS. Aims: We aimed to investigate the endothelial function and carotid atherosclerosis in healthy school-aged Tibetan male adolescents. Materials and methods: All passive smoking participants (SHS) were students were 16 years old and male, and were recruited through middle schools in Lhasa city. In total 624 subjects were accepted after excluding subjects who actively smoked. The adolescents were divided into three groups according to serum cotinine level: high cotinine group (High Group) with 205 boys, intermediate cotinine group (Intermediate Group) with 210 boys, and low cotinine group (Low Group) with 209 boys. Venous blood was sampled for the measurement of cotinine concentration, lipid profile and endothelin-1 (ET-1) quantitation. High-resolution B-mode ultrasonography was performed to evaluate carotid intimamedia thickness (cIMT) and intima smoothness. The invasive vascular endothelial function was evaluated through the measurement of flow-mediated dilation (FMD) with B-mode ultrasound and ankle-brachial index (ABI) by using a blood pressure cuff and a Doppler instrument. Results: No statistical significance was found between groups in total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglyceride, ApoA-I, systolic blood pressure, diastolic blood pressure, and heart rate (p>0.05). In the lipid profile, only apolipoprotein B (ApoB) values were different between groups: ApoB in the High Group was higher than in the Low Group (p=0.0164). Plasma ET-1 concentrations in the High Group were also much higher than in the Intermediate and Low Groups (p=0.0112, p<0.001). The cIMT and intima smoothness had deteriorated in the High Group compared with the Low Group (p<0.001 and p<0.05 respectively). FMD and ABI, which indicate vascular endothelial function, was decreased in the High Group compared with the Intermediate and Low Groups (FMD, p<0.001; ABI, p<0.001). Conclusions: SHS was associated with sub-clinical carotid atherosclerosis and endothelial dysfunction in Tibetan schoolaged male adolescents. Considering the widespread exposure to SHS and the clinical relevance of early atherosclerosis, this result is of public health importance in Tibet, where health education is not satisfactory. Data from our study emphasize the importance of endorsing smoke-free environments for adolescents.

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“…17 This pathway modulates inflammation and benefits animals in models of myocardial ischemia, 18 hepatic injury, 19 sepsis and endotoxemia, 17,20,21 IRI, [22][23][24] and the response of humans injected with lipopolysaccharide. 25 Because of its efficacy in humans and the preclinical data from human tissues, the cholinergic anti-inflammatory pathway is a promising therapeutic target. However, improved methods to stimulate this anti-inflammatory pathway are needed.…”

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confidence: 99%

Ultrasound Prevents Renal Ischemia-Reperfusion Injury by Stimulating the Splenic Cholinergic Anti-Inflammatory Pathway

Gigliotti

Huang

et al. 2013

Journal of the American Society of Nephrology

159

200

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AKI affects both quality of life and health care costs and is an independent risk factor for mortality. At present, there are few effective treatment options for AKI. Here, we describe a nonpharmacologic, noninvasive, ultrasound-based method to prevent renal ischemia-reperfusion injury in mice, which is a model for human AKI. We exposed anesthetized mice to an ultrasound protocol 24 hours before renal ischemia. After 24 hours of reperfusion, ultrasound-treated mice exhibited preserved kidney morphology and function compared with sham-treated mice. Ultrasound exposure before renal ischemia reduced the accumulation of CD11b + Ly6G high neutrophils and CD11b + F4/80 high myeloid cells in kidney tissue. Furthermore, splenectomy and adoptive transfer studies revealed that the spleen and CD4 + T cells mediated the protective effects of ultrasound. Last, blockade or genetic deficiency of the a7 nicotinic acetylcholine receptor abrogated the protective effect of ultrasound, suggesting the involvement of the cholinergic anti-inflammatory pathway. Taken together, these results suggest that an ultrasound-based treatment could have therapeutic potential for the prevention of AKI, possibly by stimulating a splenic anti-inflammatory pathway.

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Nicotine exposure altersin vivohuman responses to endotoxin

Cited by 77 publications

References 35 publications

Deficiency of IL-22 Contributes to a Chronic Inflammatory Disease: Pathogenetic Mechanisms in Acne Inversa

Deficiency of IL-22 Contributes to a Chronic Inflammatory Disease: Pathogenetic Mechanisms in Acne Inversa

Deterioration of endothelial function and carotid intima-media thickness in Tibetan male adolescents exposed to second-hand smoke

Ultrasound Prevents Renal Ischemia-Reperfusion Injury by Stimulating the Splenic Cholinergic Anti-Inflammatory Pathway

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