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. 2000 Jul 17;192(2):159–170. doi: 10.1084/jem.192.2.159

Figure 8.

Figure 8

Transgenic expression of ADA in the forestomach of ADA-deficient mice prevents adenosine and 2′-deoxyadenosine accumulation, lung inflammation, and lung histopathologies. (a) H&E-stained section of an 18-d-old control lung. (b) H&E-stained section of a 21-d-old ADA-deficient lung. (c) H&E-stained section of a 21-d-old ADA-deficient lung of a mouse expressing an ADA minigene in its forestomach. Bars, (a–c) 250 μm. (d) Adenosine and 2′-deoxyadenosine levels were quantitated in the lungs of 21-d-old control, ADA-deficient, or ADA-deficient mice expressing ADA in their forestomach (forestomach rescue). Mean values are given as nmol/mg protein ± SE; n = 3 for each. Statistical significance was determined using Student's t test analysis; *P ≤ 0.002. nd, not detected at a minimal detection limit of 0.001 nmol/mg protein. (e) Zymogram analysis showing the level of ADA enzymatic activity in the lung (L), blood (Bl), and forestomach (FS) of 21-d-old control, ADA-deficient, and ADA-deficient mice expressing ADA in their forestomach. Purine nucleoside phosphorylase (PNP) was used as a positive control.