PMID- 10629460
OWN - NLM
STAT- MEDLINE
DCOM- 20000208
LR  - 20220409
IS  - 0091-6749 (Print)
IS  - 0091-6749 (Linking)
VI  - 105
IP  - 1 Pt 1
DP  - 2000 Jan
TI  - IL-9 and its receptor in allergic and nonallergic lung disease: increased
      expression in asthma.
PG  - 108-15
AB  - BACKGROUND: Bronchial asthma is a chronic inflammatory disease associated with
      genetic components. Recently IL-9 has been reported as a candidate gene for
      asthma and to be associated with bronchial hyperresponsiveness and elevated
      levels of total serum IgE. OBJECTIVE: To investigate the contribution of IL-9 to 
      the pathogenesis of asthma, we examined the expression of IL-9 and its receptor
      (IL-9R) in bronchial tissue from subjects with atopic asthma (n = 10), chronic
      bronchitis (n = 11), and sarcoidosis (n = 9) and from atopic (n = 7) and
      nonatopic (n = 10) healthy control subjects. METHODS: Bronchial biopsy specimens 
      were examined for the presence of IL-9 and IL-9R protein and messenger RNA (mRNA)
      by immunocytochemistry and in situ hybridization, respectively. To phenotype the 
      cells expressing IL-9 in asthmatic tissue, combined in situ hybridization and
      immunocytochemistry was also performed. RESULTS: There was a highly significant
      difference (P <.001) in the expression of IL-9 mRNA in asthmatic airways (20.6
      +/- 4.0 cells/mm of basement membrane) compared with chronic bronchitis (5.6 +/- 
      4.4), sarcoidosis (2.5 +/- 1.8), atopic control subjects (7.7 +/- 2.2), and
      healthy control subjects (2.7 +/- 2.3). The number of IL-9 immunoreactive cells
      was also greater in asthmatic patients compared with the other groups (P <.05).
      Although the level of IL-9R mRNA expression did not differ in any of the groups
      (P >.05), IL-9R immunoreactivity was significantly higher in asthmatic compared
      with control subjects. Furthermore, IL-9 mRNA expression levels were also
      significantly correlated with FEV(1) (P <.05) and the airway responsiveness to
      methacholine producing a 20% fall in FEV(1) (P <. 01). The cells expressing IL-9 
      mRNA in asthmatic tissue were CD3(+) lymphocytes (68%), major basic protein(+)
      eosinophils (16%), and elastase(+) neutrophils (8%). CONCLUSION: The results of
      this study demonstrate the potential of IL-9 to be a marker for atopic asthma and
      furthermore suggest an important role for this cytokine in the pathophysiologic
      mechanisms of this disease.
FAU - Shimbara, A
AU  - Shimbara A
AD  - Meakins-Christie Laboratories, McGill University, Montreal, Quebec, Canada.
FAU - Christodoulopoulos, P
AU  - Christodoulopoulos P
FAU - Soussi-Gounni, A
AU  - Soussi-Gounni A
FAU - Olivenstein, R
AU  - Olivenstein R
FAU - Nakamura, Y
AU  - Nakamura Y
FAU - Levitt, R C
AU  - Levitt RC
FAU - Nicolaides, N C
AU  - Nicolaides NC
FAU - Holroyd, K J
AU  - Holroyd KJ
FAU - Tsicopoulos, A
AU  - Tsicopoulos A
FAU - Lafitte, J J
AU  - Lafitte JJ
FAU - Wallaert, B
AU  - Wallaert B
FAU - Hamid, Q A
AU  - Hamid QA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Allergy Clin Immunol
JT  - The Journal of allergy and clinical immunology
JID - 1275002
RN  - 0 (IL9R protein, human)
RN  - 0 (Interleukin-9)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Interleukin)
RN  - 0 (Receptors, Interleukin-9)
SB  - IM
MH  - Adult
MH  - Asthma/*metabolism
MH  - Bronchi/metabolism
MH  - Bronchial Diseases/*metabolism
MH  - Bronchitis/metabolism
MH  - Chronic Disease
MH  - Female
MH  - Humans
MH  - Hypersensitivity/*metabolism
MH  - Interleukin-9/genetics/*metabolism
MH  - Male
MH  - RNA, Messenger/metabolism
MH  - Receptors, Interleukin/genetics/*metabolism
MH  - Receptors, Interleukin-9
MH  - Reference Values
MH  - Sarcoidosis/metabolism
EDAT- 2000/01/12 00:00
MHDA- 2000/01/12 00:01
CRDT- 2000/01/12 00:00
PHST- 2000/01/12 00:00 [pubmed]
PHST- 2000/01/12 00:01 [medline]
PHST- 2000/01/12 00:00 [entrez]
AID - S0091674900999573 [pii]
AID - 10.1016/s0091-6749(00)90185-4 [doi]
PST - ppublish
SO  - J Allergy Clin Immunol. 2000 Jan;105(1 Pt 1):108-15. doi:
      10.1016/s0091-6749(00)90185-4.