[The role of I-A(b)/I-E expression in dendritic cells of acute lung injury mice]

To observe the expression of I-A(b)/I-E on circulating, lung and splenic dendritic cells (DC) in acute lung injury (ALI) mice.

Twenty-four C57BL/6 mice were randomly divided into four groups: control group, ALI 6 h, ALI 12 h and ALI 24 h group. Blood, lungs and spleens were harvested after lipopolysaccharide or phosphate butter solution administration. The expression of I-A(b)/I-E on DC was assessed by flow cytometry (FCM). IL-6 level in the lung was measured by enzyme-linked immunosorbent assay (ELISA). Lung wet weight/body weight (LW/BW) was recorded to assess lung injury. Meanwhile, pathological changes were examined under optical microscope.

(1) lipopolysaccharide-induced ALI mice resulted in a significant increase in lung LW/BW ratio. (2) Histologically, widespread alveolar wall thickening caused by edema, marked and diffuse interstitial infiltration with inflammatory cells, and severe hemorrhage in the interstitium and alveolus were observed in the ALI groups. (3) The level of IL-6 in lung tissue was significantly enhanced in ALI mice. (4) FCM analysis showed that I-A(b)/I-E expressions on lung DC [(73 ± 9)%], and splenic DC [(81 ± 8)%] were significantly higher than that on circulating DC [(24 ± 7)%;P < 0.05] in control mice. (5) In ALI mice, the expressions of I-A(b)/I-E on peripheral blood DC were (34 ± 17)% at 6 h, (51 ± 16)% at 12 h, (50 ± 17)% at 24 h respectively; I-A(b)/I-E expressions on lung DC were (82 ± 14)% at 6 h, (88 ± 6)% at 12 h, (90 ± 10)% at 24 h respectively; the expressions of I-A(b)/I-E on splenic DC were (88 ± 8)% at 6 h, (89 ± 4)% at 12 h, (93 ± 9)% at 24 h respectively, which were also significantly higher than those on the peripheral blood DC (P < 0.05). (6) The I-A(b)/I-E expressions on circulating DC in ALI mice at 12 h and 24 h was significantly higher than that on circulating DC in control mice (P < 0.05). (7) The I-A(b)/I-E expressions on lung DC and splenic DC in ALI mice at 24 h were significantly higher than those on lung DC and splenic DC in control mice (P < 0.05). (8) There was a significant correlation of I-A(b)/I-E expression on respiratory DC with the IL-6 level and lung injury score in LPS-induced ALI group (P < 0.05).

There is a dynamic characteristic in the expression I-A(b)/I-E on circulating, lung and splenic DC populations in ALI mice. I-A(b)/I-E on pulmonary DC seems to play an important role in the pathogenesis of ALI.