title: Neonatal granulocytosis is a postpartum event which is seen in the liver as well as in the blood.
abstract: In a recent series of studies, we demonstrated that stress in humans and animals, with resultant sympathetic nerve strain, induces severe granulocytosis, because granulocytes carry adrenergic receptors on the surface. Because activated granulocytes produce free radicals and superoxides, they sometimes induce tissue damage if the stress is too strong or continuous. Human neonates are also known to show high levels of granulocytes in the peripheral blood. In this study, we investigated whether such neonatal granulocytosis are a stress-associated response at birth. Both human and mouse materials, before and after birth, were used. The number of leukocytes in the blood, as well as some other factors in the serum, were measured. Although levels of granulocytes were found to be low in fetal humans and mice, they increased sharply after birth. In parallel with this postpartal granulocytosis, transaminases in sera increased transiently. In reference to results of a transient elevation in the levels of catecholamines at birth in mice, all these phenomena resemble stress-associated responses. Indeed, fatty liver and hematopoietic destruction in the liver were also observed in mice and humans. At this time, the production of inducible nitric oxide synthase (iNOS) by granulocytes in the liver was evident. These results suggest that neonatal granulocytosis is a postpartum event which results from various stresses (e.g., oxygen stress) at birth. This event may be responsible for such well-known neonatal phenomena as the termination of fetal hematopoiesis in the liver and as neonatal jaundice.
authors.affiliation: Department of Immunology, Niigata University School of Medicine, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Kawamura
authors.forename: S
authors.initials: S
authors.lastname: Toyabe
authors.forename: T
authors.initials: T
authors.lastname: Moroda
authors.forename: T
authors.initials: T
authors.lastname: Iiai
authors.forename: H
authors.initials: H
authors.lastname: Takahashi-Iwanaga
authors.forename: M
authors.initials: M
authors.lastname: Fukada
authors.forename: H
authors.initials: H
authors.lastname: Watanabe
authors.forename: H
authors.initials: H
authors.lastname: Sekikawa
authors.forename: S
authors.initials: S
authors.lastname: Seki
authors.forename: T
authors.initials: T
authors.lastname: Abo
mesh_terms: D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D002395:Catecholamines / Q000097:blood; D005234:Fatty Liver / Q000000981:diagnostic imaging; D005260:Female; D019084:Fluorescent Antibody Technique, Indirect; D006098:Granulocytes / Q000502:physiology*; D006410:Hematopoiesis / Q000502:physiology; D006801:Humans; D006931:Hyperbaric Oxygenation / Q000009:adverse effects; D007231:Infant, Newborn; D007964:Leukocytosis / Q000097:blood / Q000503:physiopathology*; D008099:Liver / Q000166:cytology* / Q000648:ultrastructure; D051379:Mice; D008807:Mice, Inbred BALB C; D019001:Nitric Oxide Synthase / Q000378:metabolism; D049590:Postpartum Period; D012333:RNA, Messenger / Q000032:analysis; D013154:Spleen / Q000000981:diagnostic imaging; D013312:Stress, Physiological / Q000097:blood / Q000503:physiopathology*; D014463:Ultrasonography
chemical_list: D002395:Catecholamines; D012333:RNA, Messenger; D019001:Nitric Oxide Synthase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase