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Exercise but not mannitol provocation increases urinary Clara cell protein (CC16) in elite swimmers.

Romberg, Kerstin LU ; Bjermer, Leif LU and Tufvesson, Ellen LU (2011) In Respiratory Medicine 105. p.31-36
Abstract
Elite swimmers have an increased risk of developing asthma, and exposure to chloramine is believed to be an important trigger factor. The aim of the present study was to explore pathophysiological mechanisms behind induced bronchoconstriction in swimmers exposed to chloramine, before and after swim exercise provocation as well as mannitol provocation. Urinary Clara cell protein (CC16) was used as a possible marker for epithelial stress. 101 elite aspiring swim athletes were investigated and urinary samples were collected before and 1 h after completed exercise and mannitol challenge. CC16, 11beta-prostaglandin (PG)F(2alpha) and leukotriene E(4) (LTE(4)) were measured. Urinary levels of CC16 were clearly increased after exercise challenge,... (More)
Elite swimmers have an increased risk of developing asthma, and exposure to chloramine is believed to be an important trigger factor. The aim of the present study was to explore pathophysiological mechanisms behind induced bronchoconstriction in swimmers exposed to chloramine, before and after swim exercise provocation as well as mannitol provocation. Urinary Clara cell protein (CC16) was used as a possible marker for epithelial stress. 101 elite aspiring swim athletes were investigated and urinary samples were collected before and 1 h after completed exercise and mannitol challenge. CC16, 11beta-prostaglandin (PG)F(2alpha) and leukotriene E(4) (LTE(4)) were measured. Urinary levels of CC16 were clearly increased after exercise challenge, while no reaction was seen after mannitol challenge. Similar to CC16, the level of 11beta-PGF(2alpha) was increased after exercise challenge, but not after mannitol challenge, while LTE(4) was reduced after exercise. There was no significant difference in urinary response between those with a negative compared to positive challenge, but a tendency of increased baseline levels of 11beta-PGF(2alpha) and LTE(4) in individuals with a positive mannitol challenge. The uniform increase of CC16 after swim exercise indicates that CC16 is of importance in epithelial stress, and may as such be an important pathogenic factor behind asthma development in swimmers. The changes seen in urinary levels of 11beta-PGF(2alpha) and LTE(4) indicate a pathophysiological role in both mannitol and exercise challenge. (Less)
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author
; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Respiratory Medicine
volume
105
pages
31 - 36
publisher
Elsevier
external identifiers
  • wos:000286863500006
  • pmid:20696561
  • scopus:78649957567
  • pmid:20696561
ISSN
1532-3064
DOI
10.1016/j.rmed.2010.07.012
language
English
LU publication?
yes
id
1be88f0f-be5c-4cc0-b78a-7288a688dbfe (old id 1665424)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/20696561?dopt=Abstract
date added to LUP
2016-04-04 09:32:17
date last changed
2022-01-29 18:21:42
@article{1be88f0f-be5c-4cc0-b78a-7288a688dbfe,
  abstract     = {{Elite swimmers have an increased risk of developing asthma, and exposure to chloramine is believed to be an important trigger factor. The aim of the present study was to explore pathophysiological mechanisms behind induced bronchoconstriction in swimmers exposed to chloramine, before and after swim exercise provocation as well as mannitol provocation. Urinary Clara cell protein (CC16) was used as a possible marker for epithelial stress. 101 elite aspiring swim athletes were investigated and urinary samples were collected before and 1 h after completed exercise and mannitol challenge. CC16, 11beta-prostaglandin (PG)F(2alpha) and leukotriene E(4) (LTE(4)) were measured. Urinary levels of CC16 were clearly increased after exercise challenge, while no reaction was seen after mannitol challenge. Similar to CC16, the level of 11beta-PGF(2alpha) was increased after exercise challenge, but not after mannitol challenge, while LTE(4) was reduced after exercise. There was no significant difference in urinary response between those with a negative compared to positive challenge, but a tendency of increased baseline levels of 11beta-PGF(2alpha) and LTE(4) in individuals with a positive mannitol challenge. The uniform increase of CC16 after swim exercise indicates that CC16 is of importance in epithelial stress, and may as such be an important pathogenic factor behind asthma development in swimmers. The changes seen in urinary levels of 11beta-PGF(2alpha) and LTE(4) indicate a pathophysiological role in both mannitol and exercise challenge.}},
  author       = {{Romberg, Kerstin and Bjermer, Leif and Tufvesson, Ellen}},
  issn         = {{1532-3064}},
  language     = {{eng}},
  pages        = {{31--36}},
  publisher    = {{Elsevier}},
  series       = {{Respiratory Medicine}},
  title        = {{Exercise but not mannitol provocation increases urinary Clara cell protein (CC16) in elite swimmers.}},
  url          = {{http://dx.doi.org/10.1016/j.rmed.2010.07.012}},
  doi          = {{10.1016/j.rmed.2010.07.012}},
  volume       = {{105}},
  year         = {{2011}},
}