Details

Autor(en) / Beteiligte

• Hilberg, Thomas
• Deigner, Hans-Peter
• Möller, Eva
• Claus, Ralf A
• Ruryk, Andriy
• Gläser, Doreen
• Landre, Julien
• Brunkhorst, Frank M
• Reinhart, Konrad
• Gabriel, Holger H. W
• Russwurm, Stefan

Titel

Transcription in response to physical stress-- clues to the molecular mechanisms of exercise-induced asthma

Ist Teil von

• The FASEB journal, 2005-09, Vol.19 (11), p.1492-1494

Ort / Verlag

United States: Federation of American Societies for Experimental Biology

Erscheinungsjahr

2005

Quelle

Wiley Online Library All Journals

Beschreibungen/Notizen

• ABSTRACTTo clarify stress‐induced immunological reactions and molecular events during exercise and the potential relevance to exercise‐induced bronchoconstriction, transcriptional responses to standardized physical stress were determined. Six healthy, young volunteers underwent an endurance exercise of 90% of their individual anaerobic threshold for 90 min. Time‐dependent alterations in the expression pattern of leukocytes from healthy, trained subjects were analyzed by DNA microarrays before and 2 h and 6 h after exercise. Starting out from a large collection of cDNA library clones comprising more than 70,000 human expressed sequence tags, we selected, designed, and immobilized oligonucleotide probes (60–70mers) for transcripts of 5000 stress‐and inflammation‐relevant genes. Exercise‐induced stress provoked changes in the expression of 433 gene activities 2 h and/or 6 h after exercise, which could be grouped into six clusters. The most prominent feature was an enhanced transcription of two genes, coding for 5‐lipoxygenase (ALOX5) and ALOX5‐activating protein. Moreover, enhanced levels of leukotriene B4 (LTB4) and LTC4 (P<0.05) were detected in plasma after exercise. Our data demonstrate that exercise alters the activities of a distinct number of genes. In particular, they possibly provide novel insights into the molecular mechanisms of exercise‐induced bronchoconstriction and suggest that enhanced transcription of ALOX5 and its activating protein together with a present predisposition of the subject critically contribute to exercise‐induced asthma.