Limits...
In vitro and in vivo characterization of ultraviolet light C-irradiated human platelets in a 2 event mouse model of transfusion.

Zhi L, Chi X, Vostal JG - PLoS ONE (2013)

Bottom Line: UVC-based technology differs from UVA or UVB-based technologies in that it uses a specific wavelength at 254 nm without the addition of any photosensitizers.Previously, it was reported that UVC irradiation induces platelet aggregation and activation.Unlike UVB-platelets, UVC-platelets did not lead to lung injury or induce MIP-2 release.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Cellular Hematology, Division of Hematology, OBRR, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland, United States of America.

ABSTRACT
UV-based pathogen reduction technologies have been developed in recent years to inactivate pathogens and contaminating leukocytes in platelet transfusion products in order to prevent transfusion-transmitted infections and alloimmunization. UVC-based technology differs from UVA or UVB-based technologies in that it uses a specific wavelength at 254 nm without the addition of any photosensitizers. Previously, it was reported that UVC irradiation induces platelet aggregation and activation. To understand if UVC-induced changes of platelet quality correlate with potential adverse events when these platelets are transfused into animals, we used a 2-event SCID mouse model in which the predisposing event was LPS treatment and the second event was infusion of UVC-irradiated platelets. We analyzed lung platelet accumulation, protein content in bronchoalveolar lavage fluid as an indication of lung injury, and macrophage inflammatory protein-2 (MIP-2) release in mice received UVC-irradiated or untreated control platelets. Our results showed UVC-irradiated platelets accumulated in lungs of the mice in a dose-dependent manner. High-doses of UVC-irradiated platelets were sequestered in the lungs to a similar level as we previously reported for UVB-irradiated platelets. Unlike UVB-platelets, UVC-platelets did not lead to lung injury or induce MIP-2 release. This could potentially be explained by our observation that although UVC treatment activated platelet surface αIIbβ3, it failed to activate platelet cells. It also suggests lung platelet accumulation and subsequent lung damage are due to different and separate mechanisms which require further investigation.

Show MeSH

Related in: MedlinePlus

UVC-irradiated HPs did not induce lung injury in the 2-event SCID mouse model.Mice were treated as described above for the 2-event SCID mouse model. Bronchoalveolar fluid (BALF) was collected 1 hour after platelet infusion and the total protein concentration in BALF was measured using BCA protein assay. Mean ± SE, n=5-10.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC3815158&req=5

pone-0079869-g005: UVC-irradiated HPs did not induce lung injury in the 2-event SCID mouse model.Mice were treated as described above for the 2-event SCID mouse model. Bronchoalveolar fluid (BALF) was collected 1 hour after platelet infusion and the total protein concentration in BALF was measured using BCA protein assay. Mean ± SE, n=5-10.

Mentions: To examine whether transfusion of UVC-irradiated human platelets in LPS-primed SCID mice was associated with lung injury and release of macrophage inflammatory protein 2 (MIP-2) as we observed with UVB-irradiated platelets [20,21], we measured the total protein concentration in bronchoalveolar lavage fluid (BALF). An increase in protein accumulation in BALF is indicative of increased lung endothelial and alveolar cell permeability and has been referred to as the hallmark of acute lung injury [28]. Consistent with the minimal changes in lung histology in response to UVC-platelets (Figure 4C), no significant difference in BALF total protein level in LPS-primed mice transfused with UVC or control platelets was observed (Figure 5). Similarly, transfusion of UVC-platelets in LPS-primed mice did not induce further increase in plasma MIP-2 levels compared to mice transfused with control platelets (Figure 6A). Although BALF MIP-2 level showed a minor rise in a few mice transfused with high-dose UVC-irradiated platelets (1.2 J/cm2), due to the variability between animals the differences did not reach statistical significance when compared to mice transfused with control platelets (Figure 6B).


In vitro and in vivo characterization of ultraviolet light C-irradiated human platelets in a 2 event mouse model of transfusion.

Zhi L, Chi X, Vostal JG - PLoS ONE (2013)

UVC-irradiated HPs did not induce lung injury in the 2-event SCID mouse model.Mice were treated as described above for the 2-event SCID mouse model. Bronchoalveolar fluid (BALF) was collected 1 hour after platelet infusion and the total protein concentration in BALF was measured using BCA protein assay. Mean ± SE, n=5-10.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3815158&req=5

pone-0079869-g005: UVC-irradiated HPs did not induce lung injury in the 2-event SCID mouse model.Mice were treated as described above for the 2-event SCID mouse model. Bronchoalveolar fluid (BALF) was collected 1 hour after platelet infusion and the total protein concentration in BALF was measured using BCA protein assay. Mean ± SE, n=5-10.
Mentions: To examine whether transfusion of UVC-irradiated human platelets in LPS-primed SCID mice was associated with lung injury and release of macrophage inflammatory protein 2 (MIP-2) as we observed with UVB-irradiated platelets [20,21], we measured the total protein concentration in bronchoalveolar lavage fluid (BALF). An increase in protein accumulation in BALF is indicative of increased lung endothelial and alveolar cell permeability and has been referred to as the hallmark of acute lung injury [28]. Consistent with the minimal changes in lung histology in response to UVC-platelets (Figure 4C), no significant difference in BALF total protein level in LPS-primed mice transfused with UVC or control platelets was observed (Figure 5). Similarly, transfusion of UVC-platelets in LPS-primed mice did not induce further increase in plasma MIP-2 levels compared to mice transfused with control platelets (Figure 6A). Although BALF MIP-2 level showed a minor rise in a few mice transfused with high-dose UVC-irradiated platelets (1.2 J/cm2), due to the variability between animals the differences did not reach statistical significance when compared to mice transfused with control platelets (Figure 6B).

Bottom Line: UVC-based technology differs from UVA or UVB-based technologies in that it uses a specific wavelength at 254 nm without the addition of any photosensitizers.Previously, it was reported that UVC irradiation induces platelet aggregation and activation.Unlike UVB-platelets, UVC-platelets did not lead to lung injury or induce MIP-2 release.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Cellular Hematology, Division of Hematology, OBRR, Center for Biologics Evaluation and Research, Food and Drug Administration, Bethesda, Maryland, United States of America.

ABSTRACT
UV-based pathogen reduction technologies have been developed in recent years to inactivate pathogens and contaminating leukocytes in platelet transfusion products in order to prevent transfusion-transmitted infections and alloimmunization. UVC-based technology differs from UVA or UVB-based technologies in that it uses a specific wavelength at 254 nm without the addition of any photosensitizers. Previously, it was reported that UVC irradiation induces platelet aggregation and activation. To understand if UVC-induced changes of platelet quality correlate with potential adverse events when these platelets are transfused into animals, we used a 2-event SCID mouse model in which the predisposing event was LPS treatment and the second event was infusion of UVC-irradiated platelets. We analyzed lung platelet accumulation, protein content in bronchoalveolar lavage fluid as an indication of lung injury, and macrophage inflammatory protein-2 (MIP-2) release in mice received UVC-irradiated or untreated control platelets. Our results showed UVC-irradiated platelets accumulated in lungs of the mice in a dose-dependent manner. High-doses of UVC-irradiated platelets were sequestered in the lungs to a similar level as we previously reported for UVB-irradiated platelets. Unlike UVB-platelets, UVC-platelets did not lead to lung injury or induce MIP-2 release. This could potentially be explained by our observation that although UVC treatment activated platelet surface αIIbβ3, it failed to activate platelet cells. It also suggests lung platelet accumulation and subsequent lung damage are due to different and separate mechanisms which require further investigation.

Show MeSH
Related in: MedlinePlus