title: Neutrophils infiltrate resistance-sized vessels of subcutaneous fat in women with preeclampsia.
abstract: We examined if there is systemic vascular inflammation and neutrophil infiltration in women with preeclampsia. Resistance-sized vessels (10 to 200 microm) of subcutaneous fat were evaluated from normal nonpregnant women, normal pregnant women, and preeclamptic women. Immunohistochemical staining was performed for: (1) interleukin-8 (IL-8), a potent neutrophil chemokine; (2) intercellular adhesion molecule-1 (ICAM-1; CD54), an endothelial cell adhesion molecule; and (3) CD66b, a neutrophil antigen. Vessels of preeclamptic patients had intense IL-8 staining in the endothelium and vascular smooth muscle, as compared with little or no staining for normal pregnant and normal nonpregnant patients. ICAM-1 was expressed on the endothelium of all patient groups. In preeclamptic patients, ICAM-1 was also expressed on vascular smooth muscle. Vessels of preeclamptic patients had significantly more CD66b staining of neutrophils than did normal pregnant or normal nonpregnant patients. There were significantly more vessels stained, more vessels with neutrophils flattened and adhered to endothelium, more vessels with neutrophils infiltrated into the intima, and more neutrophils per vessel. In conclusion, in women with preeclampsia, there was significant infiltration of neutrophils into maternal systemic vasculature associated with inflammation of the vascular smooth muscle indicated by increased expression of IL-8 and ICAM-1. Neutrophil infiltration provides a reasonable explanation for endothelial and vascular smooth muscle dysfunction in preeclampsia because neutrophils produce toxic substances, which may explain clinical symptoms.
authors.affiliation: Department of Obstetrics and Gynecology, PO Box 980034, Virginia Commonwealth University Medical Center, Richmond, VA 23298-0034, USA.
authors.forename: Courtney E
authors.initials: CE
authors.lastname: Leik
authors.forename: Scott W
authors.initials: SW
authors.lastname: Walsh
mesh_terms: D000273:Adipose Tissue / Q000098:blood supply* / Q000473:pathology; D015703:Antigens, CD; D000951:Antigens, Neoplasm / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology; D005260:Female; D058851:GPI-Linked Proteins; D006801:Humans; D007150:Immunohistochemistry; D007249:Inflammation; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D016209:Interleukin-8 / Q000378:metabolism; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology; D020556:Neutrophil Infiltration; D011225:Pre-Eclampsia / Q000276:immunology / Q000503:physiopathology*; D011247:Pregnancy; D040521:Subcutaneous Tissue / Q000098:blood supply / Q000473:pathology
chemical_list: D015703:Antigens, CD; D000951:Antigens, Neoplasm; C504120:CEACAM8 protein, human; D015815:Cell Adhesion Molecules; D058851:GPI-Linked Proteins; D016209:Interleukin-8; D018799:Intercellular Adhesion Molecule-1