| 11. |
- Georen, SK, et al.
(författare)
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Timing-dependent effects of restraint stress on eosinophilic airway inflammation in mice
- 2008
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Ingår i: Neuroimmunomodulation. - : S. Karger AG. - 1423-0216 .- 1021-7401. ; 15:3, s. 157-164
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Tidskriftsartikel (refereegranskat)abstract
- <i>Background:</i> Chronicstress has been proposed to aggravate allergic inflammation, whereas acute stress may have functional beneficial effects. The aim of this study was to investigate the influence of timing of single short restraint stress (RST) in a model of eosinophilic airway inflammation. <i>Methods:</i> The airways of ovalbumin (OVA)-sensitized mice were exposed to an intranasal OVA challenge. RST was applied in two different ways; either 2 h before (pre-stress) or after (post-stress) the OVA challenge, respectively, or as a combination of stress before and after (double-stress) the OVA challenge. One group of mice was also treated with metyrapone (ME) prior to a pre-stress challenge. The inflammatory cell response was evaluated in bronchoalveolar lavage fluid (BALF), lung and nasal tissue, as well as bone marrow. <i>Result:</i> RST applied prior to the OVA challenge (pre-stress) inhibited OVA-induced airway inflammation in BALF and lung tissue, and reduced nasal histopathology compared to unstressed mice. Given as post-stress or double-stress, RST did not affect the inflammation in BALF, lungs or nasal tissue. Pre-treatment with ME prevented the pre-challenge stress evoked decrease in inflammation in BALF and lungs. <i>Conclusion:</i> Effects of RST on eosinophilic airway inflammation appear to be strongly dependent on timing and, as could be judged from the ME inhibition pattern, also corticosterone dependent. Hypothalamic-pituitary-adrenal axis activation probably influences eosinophilic inflammation through specific sequences of compartmental activation and thereby timing effects are evident on cellular recruitment pattern during the allergic reaction.
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| 13. |
- Hoglund, CO, et al.
(författare)
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Nerve growth factor and asthma
- 2002
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Ingår i: Pulmonary pharmacology & therapeutics. - : Elsevier BV. - 1094-5539. ; 15:1, s. 51-60
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Tidskriftsartikel (refereegranskat)
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| 14. |
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| 15. |
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| 17. |
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| 20. |
- Lekander, M, et al.
(författare)
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Cytokine inhibition after glucocorticoid exposure in healthy men with low versus high basal cortisol levels
- 2009
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Ingår i: Neuroimmunomodulation. - : S. Karger AG. - 1423-0216 .- 1021-7401. ; 16:4, s. 245-250
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Tidskriftsartikel (refereegranskat)abstract
- <i>Objective:</i> The balance between glucocorticoid (GC) release and GC sensitivity in target cells is believed to be important to maintain homeostasis in the neuroendocrine control of inflammation. We investigated the impact of in vivo exposure to adrenocorticotropic hormone (ACTH) and dexamethasone (DEX) on GC sensitivity measured in vitro in healthy individuals with high versus low baseline cortisol levels. <i>Methods:</i>136 healthy male volunteers were screened twice and sorted according to their 24-hour urinary free cortisol (UFC) excretion. The 10 individuals with the highest UFC (290 ± 87 nmol/24 h) and the 10 with the lowest UFC (168 ± 34 nmol/24 h) were further tested. Measurements were performed at baseline, after a low dose (0.5 μg/1.73 m<sup>2</sup>) of ACTH challenge and after 2 weeks’ exposure to DEX (0.1 mg twice daily). GC sensitivity was assessed in vitro as the ability of DEX to inhibit lipopolysaccharide-stimulated production of the cytokines interleukin 1-β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in a whole-blood assay. <i>Results:</i>After exposure to DEX in vivo<i>,</i> inhibition of IL-6 and TNF-α decreased. Also<i>, </i>after DEX in vivo, low-cortisol men showed lower inhibition of IL-1β and IL-6, both compared to the high-cortisol group and their own baseline levels. <i>Conclusion:</i> A downregulation of GC sensitivity in leukocytes after exposure to an exogenous GC seems to occur most strongly in men with low cortisol levels.
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