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. 2015 May 15;10(5):e0125481. doi: 10.1371/journal.pone.0125481

Table 1. cSiO2 exposure increases severity of lymphocytic cell infiltration in lungs of NZBWF1 mice relative to C57Bl/6 mice.

Histopathological Lesion cSiO2 dose
NZBWF1 C57Bl/6
0.0 mg 0.25 mg 1.0 mg 0.0 mg 1.0 mg
Lymphocytic cell infiltration 0.8 ± 0.2 2.5 ± 0.3* 3.4 ± 0.2*, b 0.0 ± 0.0 2.3 ± 0.2*, a
Alveolitis 0.0 ± 0.0 1.5 ± 0.2* 2.5 ± 0.3*, a 0.0 ± 0.0 2.3 ± 0.3*, a
Alveolar proteinosis 0.0 ± 0.0 1.4 ± 0.2* 2.6 ± 0.2*, a 0.0 ± 0.0 2.6 ± 0.2*, a

Mice were graded individually for severity of lung inflammation (% of total pulmonary tissue examined) as follows: 0, no changes; 1, minimal (<10%); 2, slight (10–25%); 3, moderate (26–50%); 4, severe (51–75%) 5; very severe (>75%) of total area affected. Data are mean ± SEM (n = 8/gp). NZBWF1 mice were analyzed by One-way ANOVA on Ranks followed by Spearman rank-order correlation. C57Bl/6 mice were analyzed by Mann-Whitney Rank Sum Test. Comparisons between strains at 1.0mg cSiO2 were analyzed for statistical differences by Mann-Whitney Rank Sum Test. Asterisks indicate statistical difference between silica treatment and vehicle control (p < 0.05). Different letters indicate statistical difference in histopathological lesions between strains (p < 0.05). cSiO2 dose in NZBWF1 significantly correlated (p < 0.05) with lymphocytic cell infiltration (Spearman rank-order correlation coefficient = 0.87), alveolitis (Spearman rank-order correlation coefficient = 0.90), and alveolar proteinosis (Spearman rank-order correlation coefficient = 0.94)