PMID- 12760968
OWN - NLM
STAT- MEDLINE
DCOM- 20030710
LR  - 20171116
IS  - 1044-1549 (Print)
IS  - 1044-1549 (Linking)
VI  - 28
IP  - 6
DP  - 2003 Jun
TI  - Priming of eosinophil migration across lung epithelial cell monolayers and 
      upregulation of CD11b/CD18 are elicited by extracellular Ca2+.
PG  - 713-21
AB  - In patients with asthma, eosinophils are primed and massively infiltrate lung 
      tissues and migrate across epithelia into airways. Using blocking monoclonal 
      antibodies, we found that eosinophil transmigration across a lung epithelial cell 
      monolayer depended on the functions of alphaMbeta2 integrin CD11b/CD18. To study 
      the role of Ca2+ in eosinophil priming and transepithelial migration, we treated 
      eosinophils with eotaxin or thapsigargin (TG), reagents that increase cytoplasmic 
      free Ca2+ concentrations by receptor- or nonreceptor-mediated mechanisms, 
      respectively. Pretreatment of eosinophils with TG enhanced CD11b/CD18-dependent 
      transmigration across lung epithelium. Within minutes, TG time- and 
      dose-dependently upregulated the expression of CD11b/CD18 but did not upregulate 
      the expression of alphaL (CD11a) or beta1 (CD29) integrin. The upregulation of 
      CD11b/CD18 expression by eotaxin or TG was prevented when Ca2+ entry was blocked. 
      The priming of eosinophil transmigration by TG was also abrogated by the blockade 
      of Ca2+ entry. Our results indicate that induction of Ca2+ entry by the depletion 
      of Ca2+ from intracellular stores upregulates CD11b/CD18 expression on 
      eosinophils and primes eosinophil transmigration across lung epithelium. Both 
      responses are therefore elicited by extracellular Ca2+. We suggest that, as an 
      important priming signal for human eosinophil functional responses, 
      store-operated Ca2+ entry may be one of the underlying mechanisms of eosinophilic 
      inflammation in asthma.
FAU - Liu, Lixin
AU  - Liu L
AD  - Department of Medical Sciences, Clinical Chemistry, Uppsala University, Uppsala, 
      Sweden. lixliu@ucalgary.ca
FAU - Hakansson, Lena
AU  - Hakansson L
FAU - Ridefelt, Peter
AU  - Ridefelt P
FAU - Garcia, Rodolfo C
AU  - Garcia RC
FAU - Venge, Per
AU  - Venge P
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Am J Respir Cell Mol Biol
JT  - American journal of respiratory cell and molecular biology
JID - 8917225
RN  - 0 (CCL11 protein, human)
RN  - 0 (CD11b Antigen)
RN  - 0 (CD18 Antigens)
RN  - 0 (Chemokine CCL11)
RN  - 0 (Chemokines, CC)
RN  - 0 (Chemotactic Factors, Eosinophil)
RN  - 0 (Enzyme Inhibitors)
RN  - 67526-95-8 (Thapsigargin)
RN  - 6I3K30563S (Lanthanum)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - CD11b Antigen/*metabolism
MH  - CD18 Antigens/*metabolism
MH  - Calcium/*metabolism/pharmacology
MH  - Cell Movement/drug effects/physiology
MH  - Cells, Cultured
MH  - Chemokine CCL11
MH  - Chemokines, CC/pharmacology
MH  - Chemotactic Factors, Eosinophil/pharmacology
MH  - Chemotaxis, Leukocyte/drug effects/physiology
MH  - Enzyme Inhibitors/pharmacology
MH  - Eosinophils/*cytology/drug effects/immunology
MH  - Epithelial Cells/*cytology/drug effects/immunology
MH  - Extracellular Space
MH  - Humans
MH  - Lanthanum/pharmacology
MH  - Lung/cytology/immunology
MH  - Thapsigargin/pharmacology
MH  - Up-Regulation/drug effects
EDAT- 2003/05/23 05:00
MHDA- 2003/07/11 05:00
CRDT- 2003/05/23 05:00
PHST- 2003/05/23 05:00 [pubmed]
PHST- 2003/07/11 05:00 [medline]
PHST- 2003/05/23 05:00 [entrez]
AID - 28/6/713 [pii]
AID - 10.1165/rcmb.4771 [doi]
PST - ppublish
SO  - Am J Respir Cell Mol Biol. 2003 Jun;28(6):713-21. doi: 10.1165/rcmb.4771.