Fig. 9.
Fig. 9. Histopathological studies of lungs from wild-type, L-selectin–deficient, E/P double-selectin–null, and E/L/P triple-selectin–null mice. / Control mice (A) and L-selectin–deficient mice (B) had normal-appearing lung parenchyma. (C) In E/P double-selectin–null mice, alveolocapillary walls in tissue from inflated lungs were engorged with inflammatory cells, resulting in greatly expanded interstitial regions. (D) In contrast, the interstitial regions were remarkably more normal in the triple-null mice. Occasionally, these mice had bronchial lymphoid aggregates and a small increase in leukocytes in the alveolocapillary walls (hematoxylin and eosin, original magnification × 200). (E) Higher-power magnification (× 400) of the alveolocapillary walls from lungs of E/P double-selectin–null mice. Most of the inflammatory cells are neutrophils.

Histopathological studies of lungs from wild-type, L-selectin–deficient, E/P double-selectin–null, and E/L/P triple-selectin–null mice.

Control mice (A) and L-selectin–deficient mice (B) had normal-appearing lung parenchyma. (C) In E/P double-selectin–null mice, alveolocapillary walls in tissue from inflated lungs were engorged with inflammatory cells, resulting in greatly expanded interstitial regions. (D) In contrast, the interstitial regions were remarkably more normal in the triple-null mice. Occasionally, these mice had bronchial lymphoid aggregates and a small increase in leukocytes in the alveolocapillary walls (hematoxylin and eosin, original magnification × 200). (E) Higher-power magnification (× 400) of the alveolocapillary walls from lungs of E/P double-selectin–null mice. Most of the inflammatory cells are neutrophils.

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