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Published ahead of print on June 9, 2005, doi:10.1165/rcmb.2005-0067OC

Am. J. Respir. Cell Mol. Biol., Volume 33, Number 2, August 2005, 203-210

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Submitted on February 15, 2005
Revised on June 9, 2005

Mechanical Stretch Alters Alveolar Type II Cell Mediator Release Towards a Pro-inflammatory Pattern

Stefan Hammerschmidt1*, Hartmut Kuhn1, Ulrich Sack2, Anke Schlenska1, Christian Gessner1, Adrian Gillissen3, and Hubert Wirtz1

1 Department of Respiratory Medicine, University of Leipzig, Leipzig, Germany, 2 Department of Immunology, University of Leipzig, Leipzig, Germany, 3 Robert-Koch-Klinik, Leipzig, Germany

* To whom correspondence should be addressed. E-mail: stefan.hammerschmidt{at}t-online.de.

Increased mechanical stretch of alveolar type II (ATII) cells occurs during mechanical ventilation. The effects of three patterns of stretching rat ATII cells (frequency [min-1]-{Delta}surface area [%]: S40-13, S60-13, S40-30) were compared with those in static cultures at 12/18/24h. Cell viability and expression of COX-2, 5-LO, iNOS, eNOS were characterized. Supernatants were analyzed for eicosanoids, nitrite, cytokines and stimulatory effects on rat lymphocytes. S40-13 simulates normal breathing, the other patterns increased amplitude and frequency. There were no significant differences between S40-13 and static cultures. S60-13 only significantly increased the supernatant nitrite (11.2±1.6 versus 3.9±0.4µM at 24h). S40-30 significantly reduced the number of trypan blue excluding cells, increased the supernatant concentration of TXB2 (4.1±0,61 versus 2.2±0.36pg/ml), 6-keto-PGF1{alpha} (8.7±1.0 versus 6.7±0.52pg/ml), cysteinyl-LT (12.2±2.0 versus 6.1±0.75pg/ml) and nitrite (7.2±1.7 versus 3.9±0.4µM). S40-30 did not alter the release of TNF{alpha} and MCP-1 but significantly reduced the concentration of the anti-inflammatory IL-10 (20.8±13.3 versus 130±21.5pg/ml). Expression of COX-2/5-LO was increased/decreased; expression of iNOS/eNOS was unchanged by high amplitude stretch. Supernatants from S40-30 experiments caused lymphocyte activation measured by CD71 and CD54 surface expression. Continuing mechanical distension of ATII cells contributes to an inflammatory response by a shift in the balance of pro and anti-inflammatory mediators.




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