Animal Models of Transfusion-Related Acute Lung Injury
Section snippets
In Vitro TRALI Models
Until recently, published experimental approaches to model TRALI-mechanisms were exclusively in vitro or ex vivo studies, either based on defined cellular systems31, 32, 33 or relying on perfused explanted lungs from rats or rabbits.20,34, 35, 36 These models are described in more detail below.
In Vivo TRALI Models
The in vitro models described above mimic aspects of TRALI-like reactions in rodents but are limited compared with reproducible whole animal in vivo models. Until recently, however, no such model had been described in the peer-reviewed literature,37, 38 which perhaps is not surprising given the complexity of TRALI and the current uncertainty about its pathogenesis. Indeed, considerable investment in “trial and error”–based experimental approaches may be needed in order to tease out the
Conclusions
Whether TRALI is a distinct clinical entity or a subset syndrome of ARDS, TRALI has increased in clinical importance in recent years. Long unrecognized and existing as only scattered reports of noncardiogenic pulmonary edema after transfusions, TRALI remained largely underrecognized even after a case-series report brought it to clinicians' attention and led to coining its name 2 decades ago.30 As the threat of transfusion-transmitted viral diseases has been brought largely under control in the
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Cited by (19)
Pulmonary Complications of Transfused Blood Components
2012, Critical Care Nursing Clinics of North AmericaCitation Excerpt :Identified triggers in blood components known to induce a “second event” and subsequent TRALI in humans and animals include donor antibodies to recipient leukocyte antigens, bioactive lipids, soluble CD40-ligand, microparticles, and others.13,14 Animals develop TRALI after transfusion of blood components with high concentrations of known TRALI mediators (second event) only when administered lipopolysaccharide (first event) before transfusion.15,16 In rare situations, a “first event” is not required because certain antibody–antigen interactions (most commonly HNA-3a, an anti-neutrophil antibody) from blood components alone have enough activation energy to trigger the whole chain of events.17
Recipient T lymphocytes modulate the severity of antibody-mediated transfusion-related acute lung injury
2010, BloodCitation Excerpt :Our results do not appear to be an isolated case as it has also been shown by others that 34-1-2s induces only mild TRALI reactions in male BALB/c mice.33 Thus, the possible reasons for differences in observations between the various in vivo murine models of TRALI using 34-1-2s may relate to environmental conditions (eg, murine gut flora).34 Nonetheless, it is clear that 34-1-2s can induce a spectrum of TRALI reactions in male BALB/c mice from mild to severe depending on several factors, including mAb dose and environmental factors.
Mechanistic Understanding of Lung Inflammation: Recent Advances and Emerging Techniques
2022, Journal of Inflammation ResearchInvestigating the therapeutic effects of N-acetylcysteine decorated poly (L-lactic acid) nanoparticles on transfusion induced acute lung injury
2017, Journal of Biomaterials and Tissue EngineeringPlatelets are dispensable for antibody-mediated transfusion-related acute lung injury in the mouse
2016, Journal of Thrombosis and Haemostasis