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Results: 6

1.
Figure 3

Figure 3. Neutrophil immunohistochemistry in smoke-exposed and drug-treated mice. From: The Role of CXCR2 in Cigarette Smoke-Induced Lung Inflammation.

Lung sections were prepared as described and immunostained with an antibody specific for a neutrophil surface marker (Serotec, Oxford, UK) and counterstained with hematoxylin. Neutrophils are stained red. Very few neutrophils are present in air-exposed mice (A, B). The perivascular infiltrates in smoke-exposed mice contain many neutrophils (C), as do alveolar capillaries (E). Smoke-exposed mice treated with drug have reduced perivascular and capillary neutrophils (D, F). m, monocyte; N, neutrophil. Bar=20 μm.

T. H. Thatcher, et al. Am J Physiol Lung Cell Mol Physiol. ;289(2):L322-L328.
2.
Figure 4

Figure 4. Treatment with SCH-N significantly reduces neutrophils in lung tissue of smoke-exposed mice. From: The Role of CXCR2 in Cigarette Smoke-Induced Lung Inflammation.

To determine the number of neutrophils in tissue, lung sections (6 per mouse, 3 mice per treatment group) were immunostained to identify neutrophils, 10 random high power fields per section were counted, and the average number of neutrophils per mm3 of tissue was determined. *=significant difference from air-exposed controls; †=significant difference from smoke-exposed, vehicle-treated mice (p<0.05).

T. H. Thatcher, et al. Am J Physiol Lung Cell Mol Physiol. ;289(2):L322-L328.
3.
Figure 5

Figure 5. SCH-N does not alter the level of proinflammatory cytokines. From: The Role of CXCR2 in Cigarette Smoke-Induced Lung Inflammation.

Mice were exposed to filtered air or cigarette smoke as described, and treated with SCH-N (gray bars) or vehicle (black bars). IL-6 (A), TNF-α (B) and PGE2 (C) were measured in BAL fluid by commercially available ELISA and EIA, as described. Results shown are from a representative experiment with 6 mice per group. *=significant difference from air-exposed controls (p<0.05); the differences between smoke-exposed mice treated with vehicle or drug are not significant.

T. H. Thatcher, et al. Am J Physiol Lung Cell Mol Physiol. ;289(2):L322-L328.
4.
Figure 6

Figure 6. Treatment with SCH-N results in elevated levels of CXC chemokines. From: The Role of CXCR2 in Cigarette Smoke-Induced Lung Inflammation.

Mice were exposed to filtered air or cigarette smoke as described, and treated with SCH-N (gray bars) or vehicle (black bars). CXC chemokines MIP-2 and KC were measured in BAL fluid by commercially available ELISA. Results shown are combined from 3 experiments with a total of 12–15 mice per group. *=significant difference from air-exposed controls; †=significant difference from smoke-exposed, vehicle-treated mice (p<0.05).

T. H. Thatcher, et al. Am J Physiol Lung Cell Mol Physiol. ;289(2):L322-L328.
5.
Figure 2

Figure 2. SCH-N reduces neutrophil accumulation in lung tissue of cigarette smoke-exposed mice. From: The Role of CXCR2 in Cigarette Smoke-Induced Lung Inflammation.

Mice were exposed to filtered air or cigarette smoke and treated with SCH-N or vehicle. Lungs were inflated and fixed with formalin, and sections were stained with H&E. Air-exposed mice have normal alveoli and blood vessels (A, B). Smoke-exposed mice exhibit extensive perivascular inflammation with extravasating monocytes and neutrophils (arrows, C) and monocytes and neutrophils in the alveolar capillaries (E). Smoke-exposed mice treated with SCH-N have less perivascular inflammation (D) and greatly reduced numbers of extravasating (D) and capillary neutrophils (F). m, monocyte; N, neutrophil. Bar=20 μm.

T. H. Thatcher, et al. Am J Physiol Lung Cell Mol Physiol. ;289(2):L322-L328.
6.
Figure 1

Figure 1. Treatment with SCH-N significantly reduces cigarette smoke-induced inflammation in BAL. From: The Role of CXCR2 in Cigarette Smoke-Induced Lung Inflammation.

Mice were exposed to filtered air or cigarette smoke as described, and treated with SCH-N (gray bars) or vehicle (black bars). Differential counts were performed on BAL cells and the number of neutrophils (A), the percentage of neutrophils (B), the number of macrophages (C), the number of lymphocytes (D) and the number of eosinophils (E) are reported. Results shown are the combined results for 3 experiments with a total of 12–15 mice per group. (F) β-glucuronidase activity in BAL was measured as described for two experiments with a total of 8 mice per group. The percent inhibition by SCH-N of smoke-induced β-glucuronidase activity was calculated as 100 × ( (smoke+vehicle − control) − (smoke+drug − control))/ (smoke+vehicle − control). *=significant difference from air-exposed controls; †=significant difference from smoke-exposed, vehicle-treated mice (p<0.05).

T. H. Thatcher, et al. Am J Physiol Lung Cell Mol Physiol. ;289(2):L322-L328.

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