Results: 5

1.
Figure 1

Figure 1. Linear representation of anti-G monoclonal antibody regions of reactivity across the RSV G glycoprotein.. From: Combination Therapy Using Monoclonal Antibodies against Respiratory Syncytial Virus (RSV) G Glycoprotein Protects from RSV Disease in BALB/c Mice.

The cysteine noose region in the G protein is indicated as C, while the transmembrane and cytoplasmic domains are indicated by TM and CT, respectively. mAb 131-2G recognizes an epitope proximal to the central conserved region at a.a 1–173. mAb 130-6D recognizes an epitope within the central conserved region at a.a 174–215. mAb 232-1F reacts to an epitope outside the central conserved region at a.a. 215–298.

Hayat Caidi, et al. PLoS One. 2012;7(12):e51485.
2.
Figure 4

Figure 4. Antibody inhibition of leukocyte migration by mAbs 130-6D and 131-2G.. From: Combination Therapy Using Monoclonal Antibodies against Respiratory Syncytial Virus (RSV) G Glycoprotein Protects from RSV Disease in BALB/c Mice.

The inhibition of RSV A2 G protein – mediated leukocyte chemotaxis by anti-RSV G antibodies (130-6D and 131-2G) was determined as described in Materials and Methods. Antibody was included in the lower chamber of the chemotaxis chamber, along with purified RSV A2 G protein, at an equal concentration (1X) (22.5 µg/mL) to that of purified RSV G protein (22.5 µg/mL) up to a 50-fold concentration (50X) of mAb to purified RSV G protein. For combination mAb inhibition, 1X and 50X of each antibody were used. Each condition was assayed three times per experiment. Data is presented as an average percent inhibition of RSV A2 G protein mediated leukocyte chemotaxis ± standard deviation relative to the amount of chemotaxis induced by RSV A2 G protein alone. Asterisk indicates significant difference in inhibition (p<0.05) as determined by comparing to 131-2G (1X) or 130-6D (1X) mAb inhibition alone to combination of 131-2G and 130-6D mAbs (1X) or 130-6D (50X) mAb inhibition alone to combination of 131-2G and 130-6D mAbs (50X).

Hayat Caidi, et al. PLoS One. 2012;7(12):e51485.
3.
Figure 3

Figure 3. mAb 232-1F does not block RSV G protein induced leukocyte migration or RSV-associated pulmonary inflammation.. From: Combination Therapy Using Monoclonal Antibodies against Respiratory Syncytial Virus (RSV) G Glycoprotein Protects from RSV Disease in BALB/c Mice.

(A) mAb 232-1F was examined for its ability to block RSV G protein induced leukocyte migration in vitro compared to mAb 232-1F and mAb 131-2G. An anti-RSV F antibody (nIg) was used a negative control. Data is expressed as percent inhibition of leukocyte chemotaxis. (B) BAL cells from antibody-treated (300 µg/mouse, nIg, mAb 232-1F and mAb 131-2G) mice were harvested on days 3, 5 and day 7 post-RSV infection. The data are expressed as the mean number of BAL cells (±SE) per ml. (C) IFN-γ cytokine production (pg/mL ±SE) in cell-free BAL fluid were determined and the virus titers were determined by immunostaining plaque assay (PFU/g of tissue; ±SE) (D). Asterisks represents statistical significance (p<0.05) as determined by comparing nIg treated and mAb treated group. Representative results from two separate experiments are shown. ND indicates virus titers below the level of detection.

Hayat Caidi, et al. PLoS One. 2012;7(12):e51485.
4.
Figure 5

Figure 5. Marked reduction in RSV-associated pulmonary inflammation after early anti-RSV G mAbs combination treatment.. From: Combination Therapy Using Monoclonal Antibodies against Respiratory Syncytial Virus (RSV) G Glycoprotein Protects from RSV Disease in BALB/c Mice.

RSV-infected mice were treated with suboptimal doses of either anti-G mAb (130-6D, 150 µg/mouse) and normal Ig antibody control (nIg, 75 µg/mouse), anti-G mAb (131-2G, 75 µg/mouse) and normal Ig antibody control (nIg, 75 µg/mouse), normal Ig antibody control (nIg, 225 µg/mouse) alone or both anti-G mAbs in combination (75 µg 130-6D +150 µg 131-2G/mouse). BAL cells were harvested on days 3, 5, 7 and 11 p.i. Shown are total bronchoalveolar lavage (BAL) cell numbers (±SE) per ml (A), (B) interferon-γ (IFN-γ) (pg/ml ±SE) cytokine levels in cell-free BAL lavage fluid. (C) Virus titers (PFU/g of tissue; ± SE) and M gene expression (relative genome level equivalent PFUe/mL lung tissue ± SE) (D) in the lungs of RSV-infected mice were determined. Results are representative of three independent experiments with no fewer than three mice per time point. Asterisks indicate a significant difference (p<0.05) between nIg-treated mice and antibody-treated mice. ND indicates virus titers below the level of detection.

Hayat Caidi, et al. PLoS One. 2012;7(12):e51485.
5.
Figure 2

Figure 2. Effects of mAb 130-6D treatment on pulmonary leukocyte trafficking and RSV titers.. From: Combination Therapy Using Monoclonal Antibodies against Respiratory Syncytial Virus (RSV) G Glycoprotein Protects from RSV Disease in BALB/c Mice.

(A) The BAL cells from normal Ig antibody control (nIg, 300 µg/mouse) and anti-G mAb (mAb 130-6D; 300 µg/mouse) treated mice were harvested on days 3, 5, and day 7 p.i. The data are expressed as the mean number of BAL cells per ml (±standard error, SE). (B) Percent reduction in total CD4+, CD8+, RB6-8C5+, CD11b+, DX5+ and B220+ cell types after mAb 130-6D treatment relative to total cells type after nIg treatment at days 5 and 7 p.i. (C) The levels of IFN-γ cytokine production in BAL cell-free supernatant are expressed in pg/ml. (D) The level of RSV replication in lung tissue was evaluated by real-time RT-PCR (qRT-PCR) for M gene expression (relative genome level equivalent PFU/g of lung tissue x103) and infectious virus titers were determined by immunostaining plaque assay (PFU/g of lung tissue) (E). Asterisks indicate a significant difference (p<0.05) between nIg-treated and antibody treated mice. Results are representative of three independent experiments. ND indicates virus titers below the level of detection.

Hayat Caidi, et al. PLoS One. 2012;7(12):e51485.

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