PMID- 8730218
OWN - NLM
STAT- MEDLINE
DCOM- 19961002
LR  - 20190826
IS  - 0145-6008 (Print)
IS  - 0145-6008 (Linking)
VI  - 20
IP  - 2
DP  - 1996 Apr
TI  - Human neutrophil functions are inhibited in vitro by clinically relevant ethanol 
      concentrations.
PG  - 275-83
AB  - Neutrophils [polymorphonuclear neutrophils (PMNs)] play a pivotal role in host 
      defense in man. These defenses may be compromised, however, in alcohol users and 
      abusers. We therefore evaluated the effect of ethanol levels (12.5 to 500 mg/dl), 
      on key functions of human PMNs-chemotaxis and production of reactive oxygen 
      species-and on changes in cytosolic-free calcium ([Ca2+]i), a pivotal 
      intracellular mechanism of PMN activation. Ethanol significantly inhibited 
      chemotaxis as evaluated by formyl-methionyl-leucyl-phenylalanine (fMLP)-induced 
      upregulation of surface adhesion molecules (CD11b). fMLP-induced PMN elongation 
      was only inhibited by a very high ethanol concentration of 500 mg/dl. Production 
      of reactive oxygen species by normal PMNs was assessed by either 
      chemiluminescence (CL) for hypochlorous acid or ferricytochrome c reduction (FCR) 
      for superoxide anions. For PMN stimulated by fMLP, ethanol inhibited CL but not 
      FCR. For PMNs activated by phorbol myristate acetate, ethanol inhibited both CL 
      and FCR. Ethanol did not alter baseline [Ca2+]i, as assessed by videomicroscopy 
      using the Ca(2+)-sensing fluorescent dye Fura-2-AM, but did significantly 
      potentiate the increase in peak [Ca2+]i levels that occurs in response to 
      stimulation by fMLP. Calcium channel blockers attenuated ethanol's inhibition of 
      CL. Thus, acute in vitro ethanol, at clinically relevant concentrations, can 
      inhibit several critical aspects of PMN functions. But, in PMNs, unlike neural 
      cells, these inhibitory effects do not seem to be mediated by decreases in Ca2+ 
      influx or in [Ca2+]i.
FAU - Patel, M
AU  - Patel M
AD  - Department of Medicine, Loyola University of Chicago, Stritch School of Medicine, 
      Maywood, Illinois, USA.
FAU - Keshavarzian, A
AU  - Keshavarzian A
FAU - Kottapalli, V
AU  - Kottapalli V
FAU - Badie, B
AU  - Badie B
FAU - Winship, D
AU  - Winship D
FAU - Fields, J Z
AU  - Fields JZ
LA  - eng
GR  - AA07255/AA/NIAAA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Alcohol Clin Exp Res
JT  - Alcoholism, clinical and experimental research
JID - 7707242
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Calcium Channels)
RN  - 0 (Reactive Oxygen Species)
RN  - 3K9958V90M (Ethanol)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Calcium/metabolism
MH  - Calcium Channel Blockers/pharmacology
MH  - Calcium Channels/drug effects
MH  - Chemotaxis, Leukocyte/drug effects
MH  - Cytosol/drug effects
MH  - Dose-Response Relationship, Drug
MH  - Ethanol/*toxicity
MH  - Fluorescent Antibody Technique, Direct
MH  - Humans
MH  - In Vitro Techniques
MH  - Neutrophil Activation/drug effects
MH  - Neutrophils/*drug effects
MH  - Reactive Oxygen Species/metabolism
EDAT- 1996/04/01 00:00
MHDA- 1996/04/01 00:01
CRDT- 1996/04/01 00:00
PHST- 1996/04/01 00:00 [pubmed]
PHST- 1996/04/01 00:01 [medline]
PHST- 1996/04/01 00:00 [entrez]
AID - 10.1111/j.1530-0277.1996.tb01640.x [doi]
PST - ppublish
SO  - Alcohol Clin Exp Res. 1996 Apr;20(2):275-83. doi: 
      10.1111/j.1530-0277.1996.tb01640.x.