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Influence of hypoxia on lipopolysaccharide (LPS)‐induced chemokine CX3CL1 production by human amniotic epithelial cells (HAEC) – correlation with CX3CR1 receptor expression
Author(s) -
Szukiewicz Dariusz,
Pyzlak Michal,
Mittal Tarun Kumar,
Stangret Aleksandra
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.717.4
Subject(s) - cx3cr1 , chemokine , cx3cl1 , andrology , hypoxia (environmental) , immunology , tlr4 , lipopolysaccharide , biology , cxcl10 , chemistry , medicine , endocrinology , chemokine receptor , inflammation , organic chemistry , oxygen
Placental cytokine network includes fetal membranes. Precise autoregulation of chemokine CX3CL1 production in HAEC via CX3CL1/CX3CR1 pathway is involved in some mechanisms of both physiologic and pathologic response. Depending on the stage of pregnancy, hypoxic intrauterine environment may be beneficial or deteriorating for the utero‐placento‐fetal unit. We examined influence of low oxygen tension (5% O2) on LPS‐induced CX3CL1 production in relation to CX3CR1 expression and functional status. After normal full‐term deliveries HAEC were isolated from the amnion using trypsinization, and cultured under hypoxia (Group I; N=12) vs. normoxia (20% O2; Group II, controls; N=12). According to experimental design, LPS (1ìg/ml) or neutralizing anti‐CX3CR1 antibodies + LPS, were added at respective timepoints. Mean CX3CL1 concentration in the culture supernatant were determined by ELISA. Expression of immunostained CX3CR1 within HAEC cultures was analyzed by quantitative morphometry. Hypoxia transiently decreased (p < 0.05) CX3CL1 concentration. Blockade of CX3CR1 produced irreversible lowering in CX3CL1 production, especially in Group I (the mean 6.7‐fold decrease vs. 1.9‐fold in Group II). CX3CR1 expression was significantly augmented in Group I. The results indicate that compensatory chemokine CX3CL1 response to hypoxia may depend on CX3CR1 expression.