Display Settings:

Items per page

Results: 6

1.
Figure 2

Figure 2. From: Lack of ?-1 integrin alters lesion morphology during pulmonary Mycobacterium tuberculosis infection.

Representative Masson’s trichrome-stained lung sections from a1-null mice (A and C) and WT mice (B and D) infected with pulmonary M. tuberculosis. By day 180 of infection, collagen deposition (arrows) was greater in the lungs of the a1-null mice than in the WT strain. The total magnification is 10X for panels A and B, and 20X for panels C and D.

Jennifer L. Taylor, et al. Tuberculosis (Edinb). ;88(5):444-452.
2.
Figure 6

Figure 6. From: Lack of ?-1 integrin alters lesion morphology during pulmonary Mycobacterium tuberculosis infection.

Bacterial load in the lungs of WT and α1-null mice. Lungs (A), spleen (B) and LALN (C) were harvested over 180 days of pulmonary infection with M. tuberculosis. No differences in CFU numbers were observed between the two strains of mice over the course of the infection. Data are expressed as the mean (n = 5 mice) ± STDEV. Open circles, α1-null; closed circles, WT.

Jennifer L. Taylor, et al. Tuberculosis (Edinb). ;88(5):444-452.
3.
Figure 5

Figure 5. From: Lack of ?-1 integrin alters lesion morphology during pulmonary Mycobacterium tuberculosis infection.

Production of active MMP-9 in the lungs of WT versus α1-null mice. Lungs were harvested over a period of 180 days of pulmonary infection with M. tuberculosis and were analyzed for the production of active MMP-9. The level of active MMP-9 protein was significantly higher in the WT mouse strain beginning at day 60 of infection through day 180. Open circles, α1-null; closed circles, WT. Data are expressed as the mean (n = 5 mice) ± SEM. p values were calculated using a Student’s t-Test comparing WT versus α1-null mice at each time point; *p < 0.05.

Jennifer L. Taylor, et al. Tuberculosis (Edinb). ;88(5):444-452.
4.
Figure 4

Figure 4. From: Lack of ?-1 integrin alters lesion morphology during pulmonary Mycobacterium tuberculosis infection.

Decreased production of TNF-α in the lungs of α1-null mice. Lungs were harvested over a period of 180 days of pulmonary infection with M. tuberculosis and were analyzed by cytometric bead array for the production of TNF-α. The level of TNF-α was significantly decreased in the lung homogenates of the α1-null mice (A). Day 180 lung sections stained with anti-TNF-α antibody also showed a decrease in TNF-α staining in the α1-null mouse strain (B) compared to the WT mice (C). Open circles,α1-null; closed circles, WT. Data are expressed as the mean (n = 5 mice) ± SEM. p values were calculated using a Student’s t-Test comparing WT versus α1-null mice at each time point; *p < 0.05.

Jennifer L. Taylor, et al. Tuberculosis (Edinb). ;88(5):444-452.
5.
Figure 3

Figure 3. From: Lack of ?-1 integrin alters lesion morphology during pulmonary Mycobacterium tuberculosis infection.

Phenotypic effector T lymphocytes reside in greater numbers in the lungs of α1-null mice. Single-cell suspensions from the lungs were stained with antibodies specific for CD4 and surface activation markers CD44 (A) and CD62L (B), or intracellular IFN-γ (C). Cells were gated on lymphocytes by forward and side scatter according to their characteristic scatter profile. The number of effector CD4 T cells was higher in the α1-null mice from day 60 to day 120, and the number of IFN-γ-producing CD4 T cells was significantly higher in the α1-null mice at days 60 and 120 of infection. Open circles, α1-null; closed circles, WT. Data are expressed as the mean (n = 5 mice) ± SEM. p values were calculated using a Student’s t-Test comparing WT versus α1-null mice at each time point; *p < 0.05.

Jennifer L. Taylor, et al. Tuberculosis (Edinb). ;88(5):444-452.
6.
Figure 1

Figure 1. From: Lack of ?-1 integrin alters lesion morphology during pulmonary Mycobacterium tuberculosis infection.

Representative hematoxylin & eosin stained lung sections from α1-null mice and WT mice at days 120 and 180 of infection with M. tuberculosis. From 28 days post-infection, when lesions became apparent in both WT and α1-null mice, and at all subsequent time points except at days 120 and 180 of infection, the lesions were more numerous and tended to be more focally extensive in the WT compared to α1-null animals. By days 120 and 180, this difference was less apparent due to coalescence of lesions. The granulomatous lesions in the α1-null strain (panels A and B, respectively) were considerably smaller in size and discrete, with less tendency to coalesce compared to the lesions in the WT mouse lung (panels D and E). By day 180, there were distinct regions of cell death (panel C, box) within the granulomas in the α1-null mice, characterized by cellular and nuclear debris (C, arrow head). Alveolar septae were clearly distinct and markedly thickened in the α1-null strain (C, arrows) compared to the WT mice, in which septae were effaced by lymphocyte infiltration or dissolution (panel F). The total magnification is 20X for panels A, B, D and E, and 100X for panels C and F.

Jennifer L. Taylor, et al. Tuberculosis (Edinb). ;88(5):444-452.

Display Settings:

Items per page

Supplemental Content

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Write to the Help Desk