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Published ahead of print on December 1, 2005, doi:10.1164/rccm.200503-466OC

Am. J. Respir. Crit. Care Med., Volume 173, Number 5, March 2006, 512-518

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Submitted on March 24, 2005
Accepted on November 29, 2005

Intranasal Exposure to Stachybotrys chartarum Enhances Airway Inflammation in Allergic Mice

Marina S Leino1*, Harri T Alenius1, Nanna Fyhrquist-Vanni1, Henrik J Wolff2, Kari E Reijula3, Eeva-Liisa Hintikka3, Mirja S Salkinoja-Salonen4, Tari M.K. Haahtela5, and Mika J Makela5

1 Department of Industrial Hygiene and Toxicology, Finnish Institute of Occupational Health, Helsinki, Finland, 2 Department of Industrial Hygiene and Toxicology, Finnish Institute of Occupational Health, Helsinki, Finland; Kymenlaakso Central Hospital, Kotka, Finland; Department of Pathology, Helsinki University Central Hospital, Helsinki, Finland, 3 Uusimaa Regional Institute of Occupational Health, Helsinki, Finland, 4 Department of Applied Chemistry and Microbiology, University of Helsinki, Helsinki, Finland, 5 Department of Allergology, Helsinki University Central Hospital, Helsinki, Finland

* To whom correspondence should be addressed. E-mail: Marina.Leino{at}ttl.fi.

Rationale: Exposure to building dampness, often associated with growth of microbes such as Stachybotrys chartarum, has been linked to respiratory symptoms. We have shown previously in a murine model that exposure to Stachybotrys chartarum can induce lung inflammation characterized by infiltration of neutrophils and lymphocytes, this process being regulated by pro-inflammatory cytokines and leucocyte-attracting chemokines. Objectives: Since an atopic predisposition may influence the response to microbes, we have examined the effects of Stachybotrys chartarum on allergic mice in an experimental model. Methods: BALB/c mice were sensitized to ovalbumin by intraperitoneal injections and exposed for 3 weeks to spores of S. chartarum. Measurements and Main Results: Numbers of eosinophils and neutrophils were both drastically increased in bronchoalveolar fluid (BAL) from these mice as compared to the ovalbumin sensitized/challenged mice or those exposed to S. chartarum without ovalbumin sensitization. Histological sections showed severe granulomatous inflammatory cell infiltrates in all compartments of the lung including peribronchial, perivascular and alveolar spaces. The mRNA levels of proinflammatoric cytokines IL-1{beta} and TNF-{alpha} as well as the chemokine CCL3/MIP-1{alpha} were also markedly increased in the lungs. Despite the enhancement of the pulmonary inflammatory reaction, exposure to S. chartarum spores significantly down-regulated airway hyperresponsiveness and showed a tendency to decrease levels of Th2 cytokines in the lung. Conclusion: Exposure to Stachybotrys chartarum modulates both the inflammatory reaction and airway hyperresponsiveness, depending on the allergic status of the exposed mice.
Key words: mold, allergy, asthma, experimental model




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