Evaluation of the relationship between MARCO and CD36 single-nucleotide polymorphisms and susceptibility to pulmonary tuberculosis in a Chinese Han population

Abstract

BackgroundGene polymorphisms impact greatly on a person’s susceptibility to pulmonary tuberculosis (PTB). Macrophage receptor with collagenous structure (MARCO) and CD36 are two scavenger receptors (SRs) that can recognize Mycobacterium tuberculosis (Mtb) and play a key role in tuberculosis infection. Gene polymorphisms of MARCO and CD36 may contribute to tuberculosis risk.MethodsTo investigate whether genetic polymorphisms of MARCO and CD36 are associated with susceptibility to PTB, genomic DNA samples from patients (n = 202) and healthy controls (n = 216) were collected and analyzed by polymerase chain reaction with high-resolution melting analysis.ResultsWe studied two single nucleotide polymorphisms (SNPs) in MARCO (rs12998782 and rs17009726) and three SNPs in CD36 (rs1194182, rs3211956 and rs10499859). Rs12998782 (P = 0.018) might be associated with susceptibility to PTB. Rs1194182 (P < 0.01) and rs10499859 (P < 0.001) might be associated with resistance to PTB. Rs17009726 and rs3211956 were not associated with susceptibility/resistance to PTB.ConclusionsThese data showed that MARCO rs12998782 may increase PTB risk while two SNPs of CD36, rs1194182 and rs10499859 may reduce the risk, indicating MARCO and CD36 as important receptors in response to PTB.Electronic supplementary materialThe online version of this article (doi:10.1186/s12879-017-2595-2) contains supplementary material, which is available to authorized users.

Discrete viral E2 lysine residues and scavenger receptor MARCO are required for clearance of circulating alphaviruses

“…For example, position 252 of MARCO is known to be polymorphic in humans, and the less common variant has a decreased capacity to phagocytize bacteria in vitro (Novakowski et al, 2018). Consistent with this, SNPs within human SRs associate with differential susceptibility to various pathogens (Bowdish et al, 2013; High et al, 2016; Lao et al, 2017; Ma et al, 2011; Westhaus et al, 2017). Following alphavirus infections, human patients exhibit a high degree of variability in peak viremia and disease severity (Chow et al, 2011; de St Maurice et al, 2018; Musso et al, 2017; Thiberville et al, 2013; Vaughn et al, 2000; Waggoner et al, 2016).…”

MARCO+ lymphatic endothelial cells sequester arboviruses to limit viremia and viral dissemination

“…These finding raise the possibility that MARCO also influences disease severity in humans. The MARCO gene is highly polymorphic in humans and mice (Bowdish & Gordon, 2009), and this genetic variation has been demonstrated to influence human susceptibility to tuberculosis and respiratory syncytial virus (Bowdish et al, 2013;High et al, 2016;Lao et al, 2017;Ma et al, 2011;Thuong et al, 2016). Given our findings, it is possible that MARCO polymorphisms similarly influence disease severity following arthritogenic alphavirus infection.…”

“…For example, MARCO -/mice are impaired in their ability to clear Streptococcus pneumonia from the nasopharynx and lungs (Arredouani et al, 2004;Dorrington et al, 2013). Moreover, MARCO enhances phagocytosis of Mycobacterium tuberculosis in vitro (Bowdish et al, 2009), and MARCO polymorphisms are associated with altered susceptibility to pulmonary tuberculosis (Bowdish et al, 2013;Lao et al, 2017;Ma et al, 2011;Thuong et al, 2016). Finally, during influenza A virus infection in mice, MARCO suppresses early immunopathologic inflammatory responses, and accordingly, MARCO -/mice have increased morbidity and mortality compared with WT mice (Ghosh et al, 2011).…”

<p>The blood transcriptional signature for active and latent tuberculosis</p>

“…CD36 facilitates surfactant lipid uptake which can be exploited by M. tuberculosis for growth 43. Lao et al suggested that rs1194182 and rs10499859, two SNPs of CD36, may reduce the risk of PTB, indicating CD36 as an important biomarker for PTB 44. Hawkes et al observed that deficiency of CD36 reduces the susceptibility of mice to mycobacterial infection.…”