PMID- 9679850
OWN - NLM
STAT- MEDLINE
DCOM- 19980817
LR  - 20190723
IS  - 0091-6749 (Print)
IS  - 0091-6749 (Linking)
VI  - 102
IP  - 1
DP  - 1998 Jul
TI  - Interactions between inhalant allergen extracts and airway epithelial cells: 
      effect on cytokine production and cell detachment.
PG  - 75-85
AB  - BACKGROUND: The factors responsible for inducing or maintaining airway 
      inflammation are poorly understood. Various studies have focussed on the 
      mechanisms leading to allergic airway inflammation in patients with asthma and 
      rhinitis. The observation of local airway inflammation in nonallergic patients 
      with asthma or rhinitis, including those with nasal polyposis, suggest that 
      non-IgE-related mechanisms exist that may lead to airway inflammation. Various 
      lines of evidence suggest that epithelial cells may participate in local 
      inflammation of the airways. OBJECTIVE: This study focused on the interaction of 
      airway epithelial cells with clinically relevant inhalant allergen extracts in 
      vitro. METHODS: Cultures of airway epithelial cells were exposed to mite, Timothy 
      grass pollen, and birch pollen extracts. Production of IL-8, IL-6, 
      monocyte-chemotactic protein-1 (MCP-1), and granulocyte-macrophage 
      colony-stimulating factor and cell detachment were monitored while protease 
      inhibitors and chromatography techniques were applied to identify the factors 
      responsible for these effects. RESULTS: With the mite extracts, cytokine 
      production and cell detachment was largely dependent on protease activity. With 
      the pollen extracts, cytokine production without cell detachment seemed to be 
      independent of protease activity. CONCLUSION: These findings support the view 
      that epithelial cells may contribute to the pathogenesis of airway disease by 
      their interaction with inhalant allergen extracts. Furthermore, allergen extracts 
      may enhance airway inflammation by means other than their IgE-binding activity 
      through both protease-dependent and protease-independent mechanisms.
FAU - Tomee, J F
AU  - Tomee JF
AD  - Department of Allergology, University Hospital Groningen, The Netherlands.
FAU - van Weissenbruch, R
AU  - van Weissenbruch R
FAU - de Monchy, J G
AU  - de Monchy JG
FAU - Kauffman, H F
AU  - Kauffman HF
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 (Allergens)
RN  - 0 (Antigens, Dermatophagoides)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Glycoproteins)
RN  - 0 (Interleukin-6)
RN  - 0 (Interleukin-8)
RN  - 0 (Protease Inhibitors)
SB  - IM
MH  - Allergens/*immunology
MH  - Animals
MH  - Antigens, Dermatophagoides
MH  - Cells, Cultured
MH  - Chemical Fractionation
MH  - Chemokine CCL2/*biosynthesis
MH  - Epithelial Cells/*immunology/metabolism
MH  - Glycoproteins/*immunology
MH  - Heating
MH  - Humans
MH  - Interleukin-6/*biosynthesis
MH  - Interleukin-8/*biosynthesis
MH  - Mites/*immunology
MH  - Poaceae/immunology
MH  - Pollen/*immunology
MH  - Protease Inhibitors/pharmacology
MH  - Trees/immunology
MH  - Tumor Cells, Cultured
EDAT- 1998/07/29 00:00
MHDA- 1998/07/29 00:01
CRDT- 1998/07/29 00:00
PHST- 1998/07/29 00:00 [pubmed]
PHST- 1998/07/29 00:01 [medline]
PHST- 1998/07/29 00:00 [entrez]
AID - S0091674998002474 [pii]
AID - 10.1016/s0091-6749(98)70057-0 [doi]
PST - ppublish
SO  - J Allergy Clin Immunol. 1998 Jul;102(1):75-85. doi: 
      10.1016/s0091-6749(98)70057-0.