Mammalian cells contain two related but unique isoforms of cyclooxygenase (
COX-1 and COX-2). COX-1 is expressed constitutively in a majority of tissue
s and is involved in the production of prostaglandins (PGs) that modulate n
ormal physiologic functions. COX-2 is inducible by various stimuli and is i
nvolved in the production of PGs that modulate physiologic events in develo
pment, cell growth, and inflammation. With the exception of peribronchial g
lands and chondrocytes of peribronchial cartilage, COX-2 is not detectable
in the normal lung of nonhuman primates. We evaluated COX-2 expression by i
mmunohistochemical methods in the inflammatory lesions of two cynomolgus mo
nkeys (Macaca fascicularis) with acute severe pneumonia. Both monkeys exhib
ited acute severe bronchopneumonia; histologically, lung lesions were chara
cterized by infiltration of large numbers of neutrophils and fewer macropha
ges, mild bronchial epithelial hyperplasia, and slight type-2 pneumocyte hy
perplasia. In both monkeys, mild to marked COX-2 immunoreactivity was detec
ted within the cytoplasm of macrophages, bronchial epithelial cells, type-2
pneumocytes, and endothelial cells of blood vessels. No COX-2 immunoreacti
vity was detectable in the neutrophils that constituted >90% of the inflamm
atory cells. These observations suggest that in acute inflammatory lung les
ions in nonhuman primates 1) COX-2 is induced in the bronchial and alveolar
epithelial cells, 2) macrophages are the primary inflammatory cells that e
xhibit COX-2, and 3) neutrophils do not express COX-2.