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This study found no association of the top two associated FER variants with severity of community-acquired pneumonia. Precise characterisation of phenotypes may be required in order to unravel the genetic mechanisms predisposing to poor outcome in sepsis. https://bit.ly/3jc9SmR., Competing Interests: Conflict of interest: J. Solé-Violán has nothing to disclose. Conflict of interest: E. Hernández-Brito has nothing to disclose. Conflict of interest: J.M. Valencia-Gallardo has nothing to disclose. Conflict of interest: E. Herrera-Ramos has nothing to disclose. Conflict of interest: L. Borderías reports personal fees, nonfinancial support and other from GSK, personal fees from Allergy Therapeutics, nonfinancial support from Novartis, Boehringer and Esteve Teijin, personal fees from AstraZeneca, and nonfinancial support from Menarini, outside the submitted work. Conflict of interest: M.L. Briones has nothing to disclose. Conflict of interest: O. Rajas has nothing to disclose. Conflict of interest: J. Freixinet has nothing to disclose. Conflict of interest: L. Lorente has nothing to disclose. Conflict of interest: A. Payeras has nothing to disclose. Conflict of interest: J. Ferreres has nothing to disclose. Conflict of interest: N. Carbonell has nothing to disclose. Conflict of interest: N. González-Quevedo has nothing to disclose. Conflict of interest: J.M. González-Martin has nothing to disclose. Conflict of interest: F. Rodríguez de Castro has nothing to disclose. Conflict of interest: C. Rodríguez-Gallego has nothing to disclose., (Copyright ©ERS 2021.)

The role of mannose-binding lectin (MBL) deficiency (MBL2; XA/O and O/O genotypes) in host defences remains controversial. The surfactant proteins (SP)-A1, -A2 and -D, other collectins whose genes are located near MBL2, are part of the first-line lung defence against infection. We analysed the role of MBL on susceptibility to pneumococcal infection and the existence of linkage disequilibrium (LD) among the four genes. We studied 348 patients with pneumococcal community-acquired pneumonia (P-CAP) and 2,110 controls. A meta-analysis of MBL2 genotypes in susceptibility to P-CAP and to invasive pneumococcal disease (IPD) was also performed. The extent of LD of MBL2 with SFTPA1, SFTPA2 and SFTPD was analysed. MBL2 genotypes did not associate with either P-CAP or bacteraemic P-CAP in the case-control study. The MBL-deficient O/O genotype was significantly associated with higher risk of IPD in a meta-analysis, whereas the other MBL-deficient genotype (XA/O) showed a trend towards a protective role. We showed the existence of LD between MBL2 and SP genes. The data do not support a role of MBL deficiency on susceptibility to P-CAP or to IPD. LD among MBL2 and SP genes must be considered in studies on the role of MBL in infectious diseases.