Mariassy A T, Sielczak M W, McCray M N, Abraham W M, Wanner A
Division of Pulmonary Disease, University of Miami, Mount Sinai Medical Center, Miami Beach, FL 33140.
Am J Pathol. 1989 Nov;135(5):871-9.
Whether or not the previously reported O3-induced abnormality in the postnatal development of tracheal secretory function in lambs is accompanied by changes in epithelial cell populations and their glycoconjugate composition was determined. Six lambs were killed at birth and 12 lambs at age 2 weeks. Of the latter 12, six were exposed to O3 (1 ppm, 4 hours daily for 5 days during the 1st week of life) and five had air-sham exposures (controls). Tracheal glycoconjugates were localized in situ with lectins to detect N-acetyl-galactosamine (galNAc), alpha-D-galactose (alpha-gal), beta-D-gal(1----3)-galNAc (beta-gal), and fucose (fuc). Mean (+/- SD) epithelial cell density (cells/mm basal lamina) was 418 +/- 57 in the newborns, 385 +/- 63 in controls (P was not significant), and 342 +/- 47 in O3-exposed lambs (P less than 0.05). Mucous cell density was 87 +/- 12 in newborns, 63 +/- 10 in controls (P less than 0.05), and 76 +/- 10 in O3 exposed lambs (P was not significant). Ciliated cells remained unchanged from birth to 2 weeks (P was not significant), but decreased (P less than 0.05) in O3-exposed lambs. All counted mucous cells contained fuc and galNAc at birth and retained these residues after sham and O3 exposure. The alpha-gal-containing mucous cells declined from 97 +/- 13 to 7 +/- 1 (P less than 0.05) and beta-gal containing cells from 39 +/- 5 to 25 +/- 4 in controls. In contrast, cells containing alpha-gal 71 +/- 10 remained at newborn levels (97 +/- 13) and beta-gal-containing cells increased from 40 +/- 5 at birth to 58 +/- 8 in O3-exposed animals (P less than 0.05). It was concluded that early postnatal exposure of lambs to O3 causes a decrease in epithelial cell density, but retards the developmental decrease in the number of tracheal mucous cells and alters the lectin detectable carbohydrate composition of mucus in these cells. These developmental defects were interpreted to be the morphologic correlates of the previously shown effects of O3 on the maturation of secretory function and mucus transport.
此前报道的臭氧(O3)诱导羔羊气管分泌功能产后发育异常是否伴有上皮细胞群体及其糖缀合物组成的变化已得到确定。6只羔羊在出生时被处死,12只羔羊在2周龄时被处死。在这12只2周龄的羔羊中,6只暴露于臭氧(1 ppm,在生命的第1周每天暴露4小时,持续5天),5只进行空气假暴露(作为对照)。用凝集素对气管糖缀合物进行原位定位,以检测N-乙酰半乳糖胺(galNAc)、α-D-半乳糖(α-gal)、β-D-半乳糖(1→3)-galNAc(β-gal)和岩藻糖(fuc)。新生羔羊的平均(±标准差)上皮细胞密度(每毫米基膜的细胞数)为418±57,对照组为385±63(P无显著性差异),臭氧暴露组羔羊为342±47(P<0.05)。黏液细胞密度在新生羔羊中为87±12,对照组为63±10(P<0.05),臭氧暴露组羔羊为76±10(P无显著性差异)。从出生到2周龄,纤毛细胞数量保持不变(P无显著性差异),但在臭氧暴露组羔羊中有所减少(P<0.05)。所有计数的黏液细胞在出生时都含有岩藻糖和N-乙酰半乳糖胺,在假暴露和臭氧暴露后仍保留这些残基。对照组中含α-半乳糖的黏液细胞从97±13降至7±1(P<0.05),含β-半乳糖的细胞从39±5降至25±4。相比之下,臭氧暴露组动物中含α-半乳糖的细胞数量(71±10)保持在新生羔羊的水平(97±13),含β-半乳糖的细胞从出生时的40±5增加到58±8(P<0.05)。得出的结论是,羔羊在出生后早期暴露于臭氧会导致上皮细胞密度降低,但会延缓气管黏液细胞数量的发育性减少,并改变这些细胞中凝集素可检测到的黏液碳水化合物组成。这些发育缺陷被认为是先前所示臭氧对分泌功能成熟和黏液运输影响的形态学相关因素。