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Repression of transfusion-related acute lung injury: role of anti-cytokine and anti-chemokine Ab.

Several investigations have shown a clinical predisposition to non-hemolytic transfusion reactions, such as transfusion-related acute lung injury (TRALI), immediately after transfusions [1 4]. I determined the levels of antichemokine and anti-cytokine IgG, such as antiIL-8, anti-RANTES (regulated on activation, normal T-cell expressed and secreted), anti-macrophage inflammatory protein-1a (MIP-1a), anti-tumor necrosis factor-a (TNF-a), anti-IL-6, anti-transforming growth factor-b (TGF-b), anti-IL-11, anti-IL-1a, anti-IFN-g and antiIL-10, in 33 serum samples randomly selected from 420 blood serum samples from normal donors free from transfusion-related side-effects, using ELISA. In addition to these 33 serum samples, six anti-leukocyte Ab-positive serum samples derived from normal donors whose blood products caused TRALI in recipients were included. Four of the serum samples were anti-HLA class I Ab-negative and anti-HLA class II Ab-positive; one of these four serum samples was anti-HLA-DR15 Ab-positive (arbitrarily designated as DS15), another was anti-DR53 Ab-positive (arbitrarily designated as DS53), and the remaining two serum samples contained broadly reactive anti-DR Ab (arbitrarily designated as DS broad-1 and DS broad-2). Two serum samples were anti-HLA class I Ab-positive and anti-HLA class II Ab-negative and anti-human PMN Ag 2b (HNA-2b) Ab-positive (arbitrarily designated as DSNA-1 and DSNA-2). Of the 33 serum samples from normal donors free from transfusion-related side-effects, six were broadly reactive to both HLA class I and HLA class II (arbitrarily designated as normal human serum NHS-1, NHS-2, NHS-3, NHS-4, NHS-5 and NHS-6). Results showed that the six TRALI-related serum samples had extremely low amounts of both anti-chemokine and anti-cytokine IgG (Figure 1a, b). In contrast, NHS-1, NHS-2, NHS-3, NHS-4, NHS-5 and NHS-6, which did not induce TRALI in spite of being positive for anti-HLA class I and anti-HLA class II Ab, seemed to have rather high amounts of anti-chemokine IgG, such as anti-IL-8, anti-RANTES and anti-MIP-1a Ab (Figure 1b). The Ab to IL-8, RANTES and MIP-1a of 27 control donor plasma were all negative. It has been hypothesized that inflammatory cytokines and chemokines play pivotal roles in the development of TRALI [5,6]. These inflammatory cytokines and chemokines are thought to be released from various cells, such as PMN, monocytes and vascular endothelial cells. On the basis of this, the hypothesis was developed that suggested a high level of anti-inflammatory cytokine and chemokine Ab-containing donor blood products could neutralize detrimental cytokines and chemokines, resulting in the cessation of inflammatory reactions in recipients. Previous evidence has shown that some anti-cytokine Ab are present in normal healthy human sera [7]. The reason why some leukocyte Ab transfusions are associated with TRALI but others are not, regardless of the presence of Ab to chemokines and cytokines, is not yet clear. One explanation might be that the amounts of Ab are considerable in some recipients but not in others. For the first time, results are presented here showing that not only anti-cytokine Ab but also antichemokine Ab are present in the sera from normal healthy individuals. On the basis of this observation, we believe that we could therapeutically prevent TRALI using anti-cytokine Aband anti-chemokine Ab-containing donor blood products. The reason for the existence of