tetano
Editor, Senior Moderator
Biochem Pharmacol. 2014 Dec 31. pii: S0006-2952(14)00729-1. doi: 10.1016/j.bcp.2014.12.015. [Epub ahead of print]
[h=1]Influenza A infection attenuates relaxation responses of mouse tracheal smooth muscle evoked by acrolein.[/h] Cheah EY[SUP]1[/SUP], Mann TS[SUP]2[/SUP], Burcham PC[SUP]3[/SUP], Henry PJ[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The airway epithelium is an important source of relaxant mediators, and damage to the epithelium caused by respiratory tract viruses may contribute to airway hyperreactivity. The aim of this study was to determine whether influenza A-induced epithelial damage would modulate relaxation responses evoked by acrolein, a toxic and prevalent component of smoke. Male BALB/c mice were inoculated intranasally with influenza A/PR-8/34 (VIRUS-infected) or allantoic fluid (SHAM-infected). On day 4 post-inoculation, isometric tension recording studies were conducted on carbachol pre-contracted tracheal segments isolated from VIRUS and SHAM mice. Relaxant responses to acrolein (30μM) were markedly smaller in VIRUS segments compared to SHAM segments (2?1% relaxation vs 28?5%, n=14, p<0.01). Similarly, relaxation responses of VIRUS segments to the neuropeptide substance P (SP) were greatly attenuated (1?1% vs 47? 6% evoked by 1nM SP, n=14, p<0.001). Consistent with epithelial damage, PGE[SUB]2[/SUB] release in response to both acrolein and SP were reduced in VIRUS segments (>35% reduction, n=6, p<0.01), as determined using ELISA. In contrast, exogenous PGE[SUB]2[/SUB] was 2.8-fold more potent in VIRUS relative to SHAM segments (-logEC[SUB]50[/SUB] 7.82?0.14 vs 7.38?0.05, n=7, p<0.01) whilst responses of VIRUS segments to the β-adrenoceptor agonist isoprenaline were similar to SHAM segments. In conclusion, relaxation responses evoked by acrolein were profoundly diminished in tracheal segments isolated from influenza A-infected mice. The mechanism through which influenza A infection attenuates this response appears to involve reduced production of PGE[SUB]2[/SUB] in response to SP due to epithelial cell loss, and may provide insight into the airway hyperreactivity observed with influenza A infection.
Copyright ? 2014. Published by Elsevier Inc.
[h=4]KEYWORDS:[/h] Influenza A; acrolein; airway epithelium; mouse tracheal smooth muscle; relaxation
PMID: 25557294 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25557294
[h=1]Influenza A infection attenuates relaxation responses of mouse tracheal smooth muscle evoked by acrolein.[/h] Cheah EY[SUP]1[/SUP], Mann TS[SUP]2[/SUP], Burcham PC[SUP]3[/SUP], Henry PJ[SUP]4[/SUP].
[h=3]Author information[/h]
[h=3]Abstract[/h] The airway epithelium is an important source of relaxant mediators, and damage to the epithelium caused by respiratory tract viruses may contribute to airway hyperreactivity. The aim of this study was to determine whether influenza A-induced epithelial damage would modulate relaxation responses evoked by acrolein, a toxic and prevalent component of smoke. Male BALB/c mice were inoculated intranasally with influenza A/PR-8/34 (VIRUS-infected) or allantoic fluid (SHAM-infected). On day 4 post-inoculation, isometric tension recording studies were conducted on carbachol pre-contracted tracheal segments isolated from VIRUS and SHAM mice. Relaxant responses to acrolein (30μM) were markedly smaller in VIRUS segments compared to SHAM segments (2?1% relaxation vs 28?5%, n=14, p<0.01). Similarly, relaxation responses of VIRUS segments to the neuropeptide substance P (SP) were greatly attenuated (1?1% vs 47? 6% evoked by 1nM SP, n=14, p<0.001). Consistent with epithelial damage, PGE[SUB]2[/SUB] release in response to both acrolein and SP were reduced in VIRUS segments (>35% reduction, n=6, p<0.01), as determined using ELISA. In contrast, exogenous PGE[SUB]2[/SUB] was 2.8-fold more potent in VIRUS relative to SHAM segments (-logEC[SUB]50[/SUB] 7.82?0.14 vs 7.38?0.05, n=7, p<0.01) whilst responses of VIRUS segments to the β-adrenoceptor agonist isoprenaline were similar to SHAM segments. In conclusion, relaxation responses evoked by acrolein were profoundly diminished in tracheal segments isolated from influenza A-infected mice. The mechanism through which influenza A infection attenuates this response appears to involve reduced production of PGE[SUB]2[/SUB] in response to SP due to epithelial cell loss, and may provide insight into the airway hyperreactivity observed with influenza A infection.
Copyright ? 2014. Published by Elsevier Inc.
[h=4]KEYWORDS:[/h] Influenza A; acrolein; airway epithelium; mouse tracheal smooth muscle; relaxation
PMID: 25557294 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/pubmed/25557294