PMID- 10464825
OWN - NLM
STAT- MEDLINE
DCOM- 19991007
LR  - 20131121
IS  - 0954-6111 (Print)
IS  - 0954-6111 (Linking)
VI  - 93
IP  - 6
DP  - 1999 Jun
TI  - beta 2-agonist-induced inhibition of neutrophil chemotaxis is not associated with 
      modification of LFA-1 and Mac-1 expression or with impairment of 
      polymorphonuclear leukocyte antibacterial activity.
PG  - 416-23
AB  - Patients with chronic obstructive lung disorders often show increased 
      susceptibility to airway infections. As beta 2-adrenoceptor agonists, in addition 
      to reversing the contractile response of bronchial smooth muscles, may inhibit a 
      variety of inflammatory and immuno-effector cell functions, it is possible that 
      these drugs interfere with host defence mechanisms. The present study was 
      designed to test in vitro whether fenoterol, a short-acting beta 2-adrenoceptor 
      agonist, could modify human blood neutrophil recruitment and antimicrobial 
      activity. Pre-exposure to fenoterol significantly reduced neutrophil migration 
      towards the complement component C5a, at concentrations ranging from 10(-7) M to 
      10(-5) M, or towards lipopolysaccharide, at a concentration of 10(-5) M (P < 
      0.05, each comparison). In contrast, the drug (10(-8)-10(-5) M) did not 
      significantly modify the increased expression of lymphocyte function-associated 
      antigen (LFA-1, i.e. CD11a/CD18) the macrophage antigen-1 (Mac-1, i.e. 
      CD11b/CD18) induced by N-formylmethionylleucylphenylalanine (fMLP) (P > 0.05, 
      each comparison). Finally, incubation of neutrophils with fenoterol 
      (10(-8)-10(-5) M) did not significantly influence phagocytosis or intracellular 
      killing of bacteria (Staphylococcus aureus) or H2O2 release induced by 
      tetradecanoyl-phorbol-acetate (P > 0.1 for each comparison). These results 
      suggest that short-acting beta 2-adrenoceptor agonists, such as fenoterol, are 
      able partially to reduce neutrophil recruitment in the airways without 
      interfering with the processes involved in phagocytic activity against bacteria.
FAU - Silvestri, M
AU  - Silvestri M
AD  - Divisione di Pneumologia, Istituto G. Gaslini, Genoa, Italy.
FAU - Oddera, S
AU  - Oddera S
FAU - Lantero, S
AU  - Lantero S
FAU - Rossi, G A
AU  - Rossi GA
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Respir Med
JT  - Respiratory medicine
JID - 8908438
RN  - 0 (Adrenergic beta-Agonists)
RN  - 0 (Lymphocyte Function-Associated Antigen-1)
RN  - 0 (Macrophage-1 Antigen)
RN  - 0 (Receptors, Adrenergic)
RN  - 22M9P70OQ9 (Fenoterol)
SB  - IM
MH  - Adolescent
MH  - Adrenergic beta-Agonists/*pharmacology
MH  - Adult
MH  - Chemotaxis, Leukocyte/*drug effects
MH  - Female
MH  - Fenoterol/*pharmacology
MH  - Humans
MH  - Lung Diseases, Obstructive/*immunology
MH  - Lymphocyte Function-Associated Antigen-1/metabolism
MH  - Macrophage-1 Antigen/metabolism
MH  - Male
MH  - Neutrophils/*drug effects/*immunology
MH  - Receptors, Adrenergic/immunology
EDAT- 1999/08/28 00:00
MHDA- 1999/08/28 00:01
CRDT- 1999/08/28 00:00
PHST- 1999/08/28 00:00 [pubmed]
PHST- 1999/08/28 00:01 [medline]
PHST- 1999/08/28 00:00 [entrez]
AID - S0954-6111(99)90584-X [pii]
AID - 10.1053/rmed.1999.0584 [doi]
PST - ppublish
SO  - Respir Med. 1999 Jun;93(6):416-23. doi: 10.1053/rmed.1999.0584.