PMID- 9309982
OWN - NLM
STAT- MEDLINE
DCOM- 19971028
LR  - 20220318
IS  - 1073-449X (Print)
IS  - 1073-449X (Linking)
VI  - 156
IP  - 3 Pt 1
DP  - 1997 Sep
TI  - Relationship between IL-4 and IL-5 mRNA expression and disease severity in atopic 
      asthma.
PG  - 704-8
AB  - Atopic asthma is characterized by chronic inflammation of the bronchial mucosa in 
      which eosinophil- and immunoglobulin E (IgE)-dependent mechanisms are believed to 
      be prominent. Therefore, specific proeosinophilic mediators such as interleukin 
      (IL)-5 and essential cofactors for IgE switching in B-lymphocytes such as IL-4 
      could play a pivotal role in asthma. However, the exact role that individual 
      inflammatory mediators play in the development of the disease in humans is still 
      unknown. Using semiquantitative reverse transcriptase-polymerase chain reaction 
      amplification in bronchial biopsies from 10 atopic asthmatics, we have tested the 
      hypothesis that IL-4 and IL-5 mRNA expression relative to beta-actin mRNA 
      correlates with validated indicators of disease severity. IL-4 and IL-5 mRNA 
      copies relative to beta-actin mRNA were detected in bronchial biopsies from 
      atopic asthmatics. The numbers of IL-5 mRNA copies relative to beta-actin mRNA 
      correlated with disease severity assessed by the Aas asthma score (r = 0.70, p = 
      0.01), baseline FEV1 (r = -0.94, p = 0.001), baseline peak expiratory flow rate 
      (r = -0.77, p = 0.01), peak expiratory flow rate variability over 2 wk (r = 0.69, 
      p = 0.028), and the histamine PC20 (r = -0.72, p = 0.018). Conversely, the 
      numbers of IL-4 mRNA copies relative to beta-actin mRNA did not correlate with 
      asthma severity, but they positively correlated with total serum IgE 
      concentrations (r = -0.90, p = 0.001). Our present results support the concept 
      that IL-5 may determine asthma clinical expression and severity, and by inference 
      they support the development of IL-5 targeted therapies.
FAU - Humbert, M
AU  - Humbert M
AD  - Allergy and Clinical Immunology, Imperial College School of Medicine, National 
      Heart and Lung Institute, London, United Kingdom.
FAU - Corrigan, C J
AU  - Corrigan CJ
FAU - Kimmitt, P
AU  - Kimmitt P
FAU - Till, S J
AU  - Till SJ
FAU - Kay, A B
AU  - Kay AB
FAU - Durham, S R
AU  - Durham SR
LA  - eng
GR  - Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Respir Crit Care Med
JT  - American journal of respiratory and critical care medicine
JID - 9421642
RN  - 0 (Interleukin-5)
RN  - 0 (RNA, Messenger)
RN  - 207137-56-2 (Interleukin-4)
RN  - 37341-29-0 (Immunoglobulin E)
SB  - IM
MH  - Asthma/*immunology/*pathology
MH  - Biopsy
MH  - Bronchi/*chemistry
MH  - Case-Control Studies
MH  - Forced Expiratory Volume
MH  - Gene Expression/*immunology
MH  - Humans
MH  - Hypersensitivity, Immediate/*complications
MH  - Immunoglobulin E/immunology
MH  - Interleukin-4/*analysis
MH  - Interleukin-5/*analysis
MH  - Mucous Membrane
MH  - Peak Expiratory Flow Rate
MH  - Polymerase Chain Reaction
MH  - RNA, Messenger/*analysis
MH  - Reproducibility of Results
MH  - *Severity of Illness Index
EDAT- 1997/10/06 00:00
MHDA- 1997/10/06 00:01
CRDT- 1997/10/06 00:00
PHST- 1997/10/06 00:00 [pubmed]
PHST- 1997/10/06 00:01 [medline]
PHST- 1997/10/06 00:00 [entrez]
AID - 10.1164/ajrccm.156.3.9610033 [doi]
PST - ppublish
SO  - Am J Respir Crit Care Med. 1997 Sep;156(3 Pt 1):704-8. doi: 
      10.1164/ajrccm.156.3.9610033.