Display Settings:

Items per page
We are sorry, but NCBI web applications do not support your browser and may not function properly. More information

Results: 7

1.
Figure 3.

Figure 3. From: Mycoplasma pneumoniae CARDS Toxin Induces Pulmonary Eosinophilic and Lymphocytic Inflammation.

rCARDS toxin–induced lesions contain T cells and B cells. Lymphocytic inflammation appears in lungs of mice 7 days after treatment with rCARDS toxin. These lesions are predominantly composed of CD4+ cells (A) and CD19-positive cells (B), indicating the presence of T and B cells, respectively. Original magnification: ×20.

Jorge L. Medina, et al. Am J Respir Cell Mol Biol. 2012 June;46(6):815-822.
2.
Figure 6.

Figure 6. From: Mycoplasma pneumoniae CARDS Toxin Induces Pulmonary Eosinophilic and Lymphocytic Inflammation.

rCARDS toxin–mediated changes in pulmonary function. BALB/cJ mice were treated with CF or 700 pmol of rCARDS toxin, and changes in pulmonary function were measured using the Flexivent system at 4 and 7 days after exposure. (A) Pulmonary obstruction as measured by changes in airway resistance after a nebulized methacholine dose escalation. (B) Changes in lung compliance after a nebulized methacholine dose escalation. Diamonds represent mice treated with rCARDS toxin; squares represent mice treated with CF. Data are an average of two independent experiments with 8 to 12 animals per time point. Data are presented as the mean ± SD (*P < 0.05; **P < 0.005; ***P < 0.0005).

Jorge L. Medina, et al. Am J Respir Cell Mol Biol. 2012 June;46(6):815-822.
3.
Figure 5.

Figure 5. From: Mycoplasma pneumoniae CARDS Toxin Induces Pulmonary Eosinophilic and Lymphocytic Inflammation.

rCARDS toxin–dependent cytokine production. Mice were treated with CF or 700 pmol of rCARDS toxin, and RNA was extracted from the lungs on Days 2, 4, and 7 after exposure. qRT-PCR analysis of IL-4 (A) and IL-13 (B) mRNA expression is shown. White bars represent the CF-treated group; black bars represent the rCARDS toxin–treated group. Data are an average of two independent experiments with 8 to 10 mice per time point and are presented as fold increase relative to nontreated control mice and normalized to actin expression using the ΔΔCT method (***P < 0.005).

Jorge L. Medina, et al. Am J Respir Cell Mol Biol. 2012 June;46(6):815-822.
4.
Figure 4.

Figure 4. From: Mycoplasma pneumoniae CARDS Toxin Induces Pulmonary Eosinophilic and Lymphocytic Inflammation.

rCARDS toxin–dependent chemokine production. Mice were treated with CF or 700 pmol of rCARDS toxin. On Days 4 and 7 after exposure, bronchoalveolar lavage fluid (BALF) was obtained, and RNA was extracted from the lungs. (A) qRT-PCR analysis of CCL17 and CCL22 mRNA expression. White bars represent the CF-treated group; black bars represent the rCARDS toxin–treated group. Data represent an average of two independent experiments with 8 to 10 mice per time point and are presented as fold increase relative to nontreated control mice and normalized to actin expression using the ΔΔCT method (*P < 0.05). (B) Concentration of CCL17 and CCL22 protein in the BALF. ELISA-determined protein concentrations in the BALF. White bars represent the CF-treated group; black bars represent the rCARDS toxin–treated group. Data were obtained from the same animals used in A. Statistical significance could not be determined for the expression of CCL17 because the animals treated with CF had no detectable (N.D.) chemokine (*P < 0.05).

Jorge L. Medina, et al. Am J Respir Cell Mol Biol. 2012 June;46(6):815-822.
5.
Figure 1.

Figure 1. From: Mycoplasma pneumoniae CARDS Toxin Induces Pulmonary Eosinophilic and Lymphocytic Inflammation.

Recombinant Community-Acquired Respiratory Distress Syndrome (rCARDS) toxin–induced mucus metaplasia as detected by periodic acid Schiff (PAS) staining and quantitative real-time (qRT)-PCR. (A) Section of carrier fluid (CF)-treated lung stained with PAS at 7 days after exposure. (B) Section of rCARDS toxin–treated lung stained with PAS 7 days after exposure. Bright pink staining (black arrow) indicates the sites of mucus production. (C) Detection of Muc5AC mRNA by quantitative real-time PCR 7 days after exposure to rCARDS toxin or CF (***P < 0.005). (D and E) Sections of mouse lungs 7 days after exposure from CF or rCARDS toxin–treated animals, respectively, stained for mucin. Sections are stained with a chicken antimouse mucin antibody. (F) Quantification of the antimucin staining using the Aperio system. Data are presented as average percent positive staining ±SD. Sections from eight mice in each group were analyzed (***P < 0.0006). Original magnification of histology images: ×20.

Jorge L. Medina, et al. Am J Respir Cell Mol Biol. 2012 June;46(6):815-822.
6.
Figure 2.

Figure 2. From: Mycoplasma pneumoniae CARDS Toxin Induces Pulmonary Eosinophilic and Lymphocytic Inflammation.

rCARDS toxin–induced inflammatory changes in the lung. (A) Differentials of the cellular component of the bronchoalveolar lavage fluid 4 and 7 days after exposure to rCARDS toxin or CF. There is a significant (*P < 0.05) eosinophilia on Day 7 after exposure to rCARDS toxin. (B) rCARDS toxin–mediated increased expression of eotaxin in the BALF relative to CF control mice (*P< 0.05). (C) rCARDS toxin–dependent peribronchiolar eosinophilia as detected by H&E staining (original magnification: ×40). Inset shows high-magnification image of the eosinophils (original magnification: ×60). (D) rCARDS toxin–dependent peribronchiolar eosinophilia as detected by immunohistochemistry for eosinophil major basic protein (MBP). Positive staining is indicated by brown color (original magnification: ×40). Inset shows high-magnification image of the eosinophils (original magnification: ×60). (E) Quantification of the bronchiolar MBP immunohistochemistry using the Aperio system on Day 7 after toxin exposure (***P = 0.006). (F) Quantification of differences in average histological scores among treatment groups at Days 7, 14, 28, and 56 after toxin exposure. Scores from four blinded investigators were averaged and based on a graded scale of 1 to 5, which represented histological changes ranging from least severe to most severe. Differences between rCARDS toxin treatment and CF controls were significant at all time points (P = 0.001), and there was good agreement among evaluators (κ = 0.94–0.96).

Jorge L. Medina, et al. Am J Respir Cell Mol Biol. 2012 June;46(6):815-822.
7.
Figure 7.

Figure 7. From: Mycoplasma pneumoniae CARDS Toxin Induces Pulmonary Eosinophilic and Lymphocytic Inflammation.

Dependence of rCARDS toxin–mediated changes in pulmonary function and histopathology on CD4+ T cells. BALB/cJ mice were injected intraperitoneally with 250 μg of rat anti-CD4 IgG antibody or 250 μg of irrelevant rat IgG 1 day before inoculation with 700 pmol rCARDS toxin. Mice were treated again with rat anti-CD4 or irrelevant rat IgG on Day 3 after rCARDS toxin exposure. (A) rCARDS toxin–dependent changes in airway resistance were measured by Flexivent. Animals lacking CD4+ T cells have significantly reduced changes in airway resistance and compliance. Diamonds represent mice treated with rCARDS toxin and rat anti-CD4 IgG; squares represent mice treated with rCARDS and irrelevant rat IgG. Data represent the mean ± SD from two independent experiments with a total of 10 to 15 mice per treatment group (*P < 0.02; ***P ≤ 0.002). (B) Mice treated with anti-CD4 antibodies do not develop peribronchiolar and perivascular inflammatory lesions characteristic of rCARDS toxin exposure (8). Note the large lymphoid aggregates in the rat IgG control lungs (black arrows) that are absent in the anti-CD4–treated animals. (C) Depletion of CD4+ T cells abolishes rCARDS toxin–induced expression of IL-4 and IL-13 mRNA in the lungs as determined by qRT-PCR (***P < 0.005). (D) Mice treated with anti-CD4 antibodies produce less mucus at the bronchiolar epithelium. Note the bright pink staining in the rat IgG control mice (black arrow) that is absent in the anti-CD4–treated mice. (E) Decreased Muc5AC mRNA expression in anti-CD4–treated animals was determined by qRT-PCR (***P < 0.005). (F) Anti-CD4–treated mice have less mucin protein in the lungs after rCARDS treatment compared with rat IgG–treated animals. Quantification of the antimucin staining using the Aperio system is shown. Data are presented as average percent positive staining ±SD. Sections from eight mice in each group were analyzed (*P = 0.03). Data from all other experiments are representative of two independent experiments with 10 to 15 mice. Original magnification of histology images: ×20.

Jorge L. Medina, et al. Am J Respir Cell Mol Biol. 2012 June;46(6):815-822.

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