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Blood, Vol. 93 No. 6 (March 15), 1999:
pp. 1843-1850
RAPID COMMUNICATION
Human Immunodeficiency Virus-1-Infected Macrophages Induce
Inducible Nitric Oxide Synthase and Nitric Oxide (NO)
Production in Astrocytes: Astrocytic NO as a Possible Mediator of
Neural Damage in Acquired Immunodeficiency Syndrome
Kotaro Hori,
Parris R. Burd,
Keizo Furuke,
Joseph Kutza,
Karis A. Weih, and
Kathleen A. Clouse
From the Division of Cytokine Biology and the Division of Cellular
and Gene Therapies, Center for Biologics Evaluation and Research, Food
and Drug Administration, Rockville, MD.
Nitric oxide (NO) plays an important role in normal neural cell
function. Dysregulated or overexpression of NO contributes to
neurologic damage associated with various pathologies, including human
immunodeficiency virus (HIV)-associated neurological disease. Previous
studies suggest that HIV-infected monocyte-derived macrophages (MDM)
produce low levels of NO in vitro and that inducible nitric oxide
synthase (iNOS) is expressed in the brain of patients with neurologic
disease. However, the levels of NO could not account for the degree of
neural toxicity observed. In this study, we found that induction of
iNOS with concomitant production of NO occurred in primary human
astrocytes, but not in MDM, when astrocytes were cocultured with
HIV-1-infected MDM. This coincided with decreased HIV replication in
infected MDM. Supernatants from cocultures of infected MDM and
astrocytes also stimulated iNOS/NO expression in astrocytes, but
cytokines known to induce iNOS expression (interferon- , interleukin-1 , and tumor necrosis factor- ) were not detected. In
addition, the recombinant HIV-1 envelope protein gp41, but not rgp120,
induced iNOS in cocultures of uninfected MDM and astrocytes. This
suggests that astrocytes may be an important source of NO production
due to dysregulated iNOS expression and may constitute one arm of the
host response resulting in suppression of HIV-1 replication in the
brain. It also leads us to speculate that neurologic damage observed in
HIV disease may ensue from prolonged, high level production of NO.
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