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Submitted on August 8, 2005
Accepted on October 18, 2005
Howard Florey Institute of Experimental Physiology & Medicine (I.M., G.W.T., C.S.S.), University of Melbourne, Parkville, Victoria 3010; and Murdoch Children's Research Institute (N.R.S., S.G.R., M.L.K.T.), Royal Childrens Hospital, Parkville, Victoria 3052, Australia
* To whom correspondence should be addressed. E-mail: c.samuel{at}hfi.unimelb.edu.au or mimi.tang{at}rch.org.au.
We examined the relationship between relaxin (a peptide hormone which stimulates collagen degradation), airway fibrosis, other changes of airway remodelling, and airway hyperresponsiveness (AHR) in an animal model of allergic airways disease (AAD). Eight to ten week old relaxin gene-knockout (RLX-/-) and wild-type (RLX+/+) mice were sensitized with ovalbumin (OVA) or saline i.p at day 0 and 14 and challenged three times per week for six weeks with nebulized 2.5% OVA or saline. Saline-treated control RLX+/+ and RLX-/- mice had equivalent collagen expression and baseline airway responses. OVA-treated RLX-/- mice developed airway inflammation equivalent to that in OVA-treated RLX+/+ mice. However, OVA-treated RLX-/- mice had markedly increased lung collagen deposition as compared with OVA-treated RLX+/+ and saline-treated mice (all P < 0.05). Collagen was predominantly deposited in the subepithelial basement membrane region and submucosal regions in both OVA-treated RLX+/+ and RLX-/- mice. The increased collagen measured in OVA-treated RLX-/- mice was associated with reduced matrix metalloproteinase (MMP)-9 (P < 0.02) expression and failure to up-regulate MMP-2 expression, compared with levels in OVA-treated RLX+/+ mice. Goblet cell numbers were equivalent in OVA-treated RLX-/- and RLX+/+ mice and increased compared with saline-treated animals. Both RLX+/+ and RLX-/- OVA-treated mice developed similar degrees of AHR following OVA-treatment. These findings demonstrate a critical role for relaxin in the inhibition of lung collagen deposition during an allergic inflammatory response. Increased deposition of collagen per se did not influence airway epithelial structure or AHR.
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