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Background  Urinary Schistosomiasis is a neglected tropical disease endemic in many sub Saharan -African countries. Collectin Kidney 1 (CL-K1, encoded by  COLEC11  on chromosome 2p25.3), a member of the vertebrate C-type lectin super family, has recently been identified as pattern-recognition molecule (PRR) of the lectin complement pathway. CL-K1 is preferentially expressed in the kidneys, but also in other organs and it is considered to play a role in host defense to some infectious agents. Schistosome teguments are fucosylated and CL-K1 has, through its collagen-like domain, a high binding affinity to fucose.    Methodology/Principal Findings  We utilized a Nigerian study group consisting of 167  Schistosoma haematobium  infected individuals and 186 matched healthy subjects, and investigated the contribution of CL-K1 deficiency and of  COLEC11  polymorphisms to infection phenotype. Higher CL-K1 serum levels were associated with decreased risk of schistosome infection ( P corr   = 0.0004). CL-K1 serum levels were differentially distributed between the  COLEC11  genotypes and haplotypes observed. The non-synonymous variant  p . R216H  was associated with the occurrence of schistosomiasis (OR = 0.44, 95%CI = 0.22–0.72,  P corr   = 0.0004). The reconstructed  COLEC11*TCCA  haplotypes were associated with higher CL-K1 serum levels ( P  = 0.002) and with decreased schistosomiasis (OR = 0.38, 95%CI = 0.23–0.63,  P corr   = 0.0001).    Conclusions  In agreement with findings from our earlier published study, our findings support the observation that CL-K1 and their functional variants may be host factors associated with protection in schistosomiasis and may be a useful marker for further investigations.

Lectin Complement Protein Collectin 11 (CL-K1) and Susceptibility to Urinary Schistosomiasis