Peripheral blood monocyte-derived chemokine blockade prevents murine transfusion-related acute lung injury (TRALI)

McKenzie, Craig R. M.; Kim, Michael; Singh, Tarandeep; Milev, Youli; Freedman, J.; Semple, John W.

doi:10.1182/blood-2013-11-536755

Cited by 56 publications

(69 citation statements)

References 41 publications

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“…The current findings show that both CRP and 34-1-2s alone induce MIP-2 production in vivo, although neither is sufficient to induce TRALI. The source of MIP-2 in our study is unknown, but our previous work suggests that the primary source of the chemokine is monocytes, 15 and, of interest, others have shown that CRP can augment the secretion of IL-8 by human peripheral blood monocytes.…”

Section: Discussionmentioning

confidence: 83%

“…It shares the same extracellular loop reactive 1 motif (Glu-Leu-Arg) for the chemoattractant properties of IL-8. 31, 32 We previously found that MIP-2 plays a central role in 34-1-2s-mediated TRALI-induction severe combined immunodeficiency mice, 15 and because IL-8 is associated with an increased risk in human TRALI, 20,21 we measured MIP-2 values in our BALB/c TRALI model. The current findings show that both CRP and 34-1-2s alone induce MIP-2 production in vivo, although neither is sufficient to induce TRALI.…”

Section: Discussionmentioning

confidence: 97%

“…Furthermore, we demonstrated that TRALI induction was due to 34-1-2s binding to its cognate MHC class I antigens on monocytes, activating them to secrete macrophage inflammatory protein-2 (MIP-2), the murine equivalent of human interleukin-8 (IL-8), which was associated with pulmonary neutrophil recruitment. 15 This event initiated subsequent lung damage in an Fc-dependent process. 15 In the original study, TRALI induction in BALB/c mice injected with 34-1-2s was robust and significant lung damage was observed.…”

Section: Introductionmentioning

confidence: 99%

“…15 This event initiated subsequent lung damage in an Fc-dependent process. 15 In the original study, TRALI induction in BALB/c mice injected with 34-1-2s was robust and significant lung damage was observed. 5 Subsequently, however, TRALI-induction by 34-1-2s was lost and only BALB/c mice administered with the bacterial endotoxin lipopolysaccharide (LPS) succumbed to TRALI.…”

Section: Introductionmentioning

confidence: 99%

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C-reactive protein enhances murine antibody–mediated transfusion-related acute lung injury

Kapur

Kim

Shanmugabhavananthan

et al. 2015

Blood

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Key Points• CRP enhances antibodymediated lung damage when infused into TRALI-resistant mice.• CRP and TRALI-inducing antibodies generate a synergistic increase in MIP-2 production and pulmonary neutrophil accumulation in vivo.Transfusion-related acute lung injury (TRALI) is a syndrome of respiratory distress triggered by blood transfusions and is the leading cause of transfusion-related mortality. TRALI has primarily been attributed to passive infusion of HLA and/or human neutrophil antigen antibodies present in transfused blood products, and predisposing factors such as inflammation are known to be important for TRALI initiation. Because the acute-phase protein C-reactive protein (CRP) is highly upregulated during infections and inflammation and can also enhance antibody-mediated responses such as in vitro phagocytosis, respiratory burst, and in vivo thrombocytopenia, we investigated whether CRP affects murine antibody-mediated TRALI induced by the anti-major histocompatibility complex antibody 34-1-2s. We found that BALB/c mice injected with 34-1-2s or CRP alone were resistant to TRALI, however mice injected with 34-1-2s together with CRP had significantly enhanced lung damage and pulmonary edema. Mechanistically, 34-1-2s injection with CRP resulted in a significant synergistic increase in plasma levels of the neutrophil chemoattractant macrophage inflammatory protein-2 (MIP-2) and pulmonary neutrophil accumulation. Importantly, murine MIP-2 is the functional homolog of human interleukin-8, a known risk factor for human TRALI. These results suggest that elevated in vivo CRP levels, like those observed during infections, may significantly predispose recipients to antibodymediated TRALI reactions and support the notion that modulating CRP levels is an effective therapeutic strategy to reduce TRALI severity. (Blood. 2015;126(25):2747-2751 Introduction Transfusion-related acute lung injury (TRALI) is characterized by respiratory distress following blood transfusions and is the leading cause of transfusion-related mortality.1,2 Approximately 80% of TRALI cases are associated with HLA-or human neutrophil antigen-specific antibodies present in donor blood.3,4 A 2-hit model was hypothesized to underlie antibody-mediated TRALI where the first hit comprises patient predisposing factors, such as inflammation, and the second hit is due to antibodies in the transfused blood.1 The pathogenesis of antibody-mediated TRALI, however, is still poorly understood, and controversy has arisen using animal models. For example, several cell types have been implicated in inducing lung damage by the TRALI-inducing anti-major histocompatibility complex (MHC) class I antibody 34-1-2s.5 Neutrophils were originally thought to be stimulated by 34-1-2s to produce reactive oxygen species that damaged the pulmonary endothelium in an Fc-dependent manner.1,5-13 Strait et al, 14 however, showed that neutrophil involvement was limited and that activated endothelial cells and complement interactions were the primary events in TRALI induction. Furth...

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Section: Discussionmentioning

confidence: 83%

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

C-reactive protein enhances murine antibody–mediated transfusion-related acute lung injury

Kapur

Kim

Shanmugabhavananthan

et al. 2015

Blood

Self Cite

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show abstract

“…2 The pathogenesis is still poorly understood but several cellular processes have been described such as neutrophil activation, pulmonary endothelial barrier function disruption, and the involvement of monocytes. [4][5][6] In addition, several TRALI risk factors have been described in recipients which include increased levels of interleukin-8 (IL-8), liver surgery, chronic alcohol abuse, shock, higher peak airway pressure while being mechanically ventilated, smoking, and positive intravascular fluid balance. 7 In a prepost study, IL-6 and IL-8 were found to be elevated before and after transfusion in patients with TRALI.…”

mentioning

confidence: 99%