Document 0638
 DOCN  M95A0638
 TI    Nitric oxide production by alveolar macrophages from newborn versus
       infant and adult rats. American Pediatric Society 104th annual meeting
       and Society for Pediatric Research 63rd annual meeting; 1994 May 2-5;
       Seattle.
 DT    9510
 AU    Sherman MP; Wong VZ; Univ. of Kansas, Kansas City, USA.
 SO    Pediatr AIDS HIV Infect. 1994 Oct;5(5):315 (unnumbered abstract). Unique
       Identifier : AIDSLINE AIDS/95330406
 AB    Human immunodeficiency virus (HIV) infection of newborns progresses to
       AIDS more rapidly than infection in later life. Since nitric oxide (NO)
       blocks lymphocyte proliferation and HIV gp120 stimulates NO production
       by human macrophages (M phi), we postulate that excessive NO production
       by newborn M phi causes rapid HIV disease progression during infancy.
       After interferon-gamma and lipopolysaccharide stimulation of cultured
       alveolar M phi lavaged from 3-day-old, 10-day-old, and adult rats, NO
       production was measured as its end products: NO2- [Griess reaction],
       NO3- [nitrate reductase assay], and citrulline [diacetylmonoxime +
       antipyrine colorimetric method]. Micromolar concentrations of NO2- and
       NO3- in supernatants were: 114 +/- 4* & 59 +/- 15 (3-day), 40 +/- 9 & 37
       +/- 6 (10-day-old), and 36 +/- 5 & 42 +/- 6 (adult) [mean +/- SEM; *= p
       < 0.05 v. 10-day and adult.]. Citrulline was 80-100% higher in
       supernatants of 3-day-old M phi versus that produced by older M phi.
       Stimulated superoxide (O2-) generation [ferricytochrome c reduction
       method] was also measured to exclude that O2- produced by older M phi
       did not react with NO and prevent its detection. O2- production
       (nmol/10(6) AM/10 min) was: 18 +/- 1 (3-day), 15 +/- 1 (10-day), and 16
       +/- 2 (adult). We conclude that activated lung M phi of 3-day-old rats
       produce significantly more NO than their older counterparts. We
       speculate that excessive NO may explain CD4 T-cell dysfunction and loss
       in AIDS and rapid progression of HIV infection to AIDS during infancy.
 DE    Acquired Immunodeficiency Syndrome/PHYSIOPATHOLOGY  Aging/*METABOLISM
       Animal  Cells, Cultured  Citrulline/METABOLISM  Macrophages,
       Alveolar/*METABOLISM  Nitrates/METABOLISM  Nitric Oxide/*METABOLISM
       Nitrous Oxide/METABOLISM  Rats  Superoxides/METABOLISM  MEETING ABSTRACT
       JOURNAL ARTICLE

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