Is mannose-binding lectin deficiency associated with infection due to Gram-positive bacteria?

To the Editor—We read with great interest the article by Eisen et al. [1], in which the authors report an ambitious multivariable analysis of several articles on the impact of mannose-binding lectin (MBL) deficiency on the outcome of severe bacterial infection and sepsis. Although genetic polymorphisms in the genes encoding different molecules of the innate immune system have been associated with increased mortality in patients with severe sepsis and septic shock [2–4], examination of the association of MBL deficiency with death among patients in the intensive care unit has yielded conflicting results [5, 6]. In fact, in the study by Eisen et al. [1], only a trend toward an increased risk of death among MBL-deficient patients in the intensive care unit was observed , which could be attributable to the high heterogenicity of the patients included in these studies. Similar conflicting results are observed when the relationship between a microorganism or a group of microorganisms and MBL deficiency is analyzed. Although some studies have found an association between infection due to gram-positive bacteria and MBL deficiency [6], other studies have observed a link between infection due to gram-negative bacteria and MBL deficiency [7]. With regard to this question, in the study by Eisen et al. [1], an increased risk of death was observed for patients with low serum levels of MBL and pneumococcal infection. It is worth mentioning that most of the articles that have focused on this topic have not been able to establish an association between the incidence or outcome of Streptococcus pneumoniae infection and the existence of MBL deficiency. In fact, in vitro studies have demonstrated that S. pneumoniae has a low binding capacity to MBL [8]. Additionally, the level of expression of the capsule of S. pneumoniae, which has a negative impact on MBL binding, may vary during different phases of the infection [9]. Finally, minor differences in the sugar-array composition of the membranes of S. pneumoniae, which is responsible for the different serotypes of the bacteria, may account for additional differences in the ability of S. pneumoniae to bind to MBL. In the same study by Eisen et al. [1], no significant association was found between MBL deficiency and death due to Staphylococcus aureus infection, probably because of the small number of patients with this condition who were included in the analysis. In vitro studies have demonstrated that S. aureus binds to MBL with high …