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Current endeavour focuses on human genetic factors that contribute to susceptibility to or protection from tuberculosis (TB). Monocytes are crucial in containingMycobacterium tuberculosisinfection, and the monocyte chemoattractant protein-1 (MCP-1) cytokine plays a role in their recruitment to the site of infection. The G allele of theMCP-1promoter polymorphism at position −2581 relative to the ATG transcription start codon has been described to be associated in Mexican and Korean TB patients with increased susceptibility to TB. We genotyped this and additionalMCP-1variants in sample collections comprising more than 2000 cases with pulmonary TB and more than 2300 healthy controls and 332 affected nuclear families from Ghana, West Africa, and more than 1400 TB patients and more than 1500 controls from Russia. In striking contrast to previous reports,MCP-1−2581G was significantly associated with resistance to TB in cases versus controls [odds ratio (OR) 0.81, correctedP-value (P  corr) = 0.0012] and nuclear families (OR 0.72,P  corr= 0.04) and not with disease susceptibility, whereas in the Russian sample no evidence of association was found (P= 0.86). Our and other results do not support an association ofMCP-1−2581 with TB. In the Ghanaian population, eight additionalMCP-1polymorphisms were genotyped.MCP-1−362C was associated with resistance to TB in the case–control collection (OR 0.83,P  corr= 0.00017) and in the affected families (OR 0.7,P  corr= 0.004). Linkage disequilibrium (LD) and logistic regression analyses indicate that, in Ghanaians, the effect results exclusively from theMCP-1−362 variant, whereas the effect of −2581 may in part be explained by its LD with −362.

MCP-1 promoter variant −362C associated with protection from pulmonary tuberculosis in Ghana, West Africa