Functional Mannose-binding Lectin Research Articles

Bacterial surface display of human lectins in Escherichia coli.

Lectin-glycan interactions sustain fundamental biological processes involved in development and disease. Owing to their unique sugar-binding properties, lectins have great potential in glycobiology and biomedicine. However, their relatively low affinities and broad specificities pose a significant challenge when used as analytical reagents. New approaches for expression and engineering of lectins are in demand to overcome current limitations. Herein, we report the application of bacterial display for the expression of human galectin-3 and mannose-binding lectin in Escherichia coli. The analysis of the cell surface expression and binding activity of the surface-displayed lectins, including point and deletion mutants, in combination with molecular dynamics simulation, demonstrate the robustness and suitability of this approach. Furthermore, the display of functional mannose-binding lectin in the bacterial surface proved the feasibility of this method for disulfide bond-containing lectins. This work establishes for the first time bacterial display as an efficient means for the expression and engineering of human lectins, thereby increasing the available toolbox for glycobiology research.

Analysis of Mannose-Binding Lectin Protein Levels and their MIC Profile in Patients with Dermatophytosis.

Analysis of Mannose-Binding Lectin Protein Levels and their MIC Profile in Patients with Dermatophytosis.

Mannose-binding lectin levels and MBL2 gene polymorphisms are associated with dengue infection in Brazilian children at the early ages

BackgroundThe mannose-binding lectin (MBL) plays an important role in innate immunity. Genetically determined variations in serum levels of MBL may influence the susceptibility and clinical outcome of dengue infection in early life. MethodsWe investigated the MBL2 gene polymorphisms and serum levels of MBL (total and functional) in children with asymptomatic (n=17) and symptomatic (n=29) primary dengue infections and age-matched uninfected children (n=84) enrolled in a birth cohort with dengue in Brazil. Polymorphisms of the MBL2 gene were assessed by reverse transcription-polymerase chain reaction (RT-PCR), whereas the enzyme-linked immunosorbent assay (ELISA) was used to quantify serum levels of MBL. ResultsWe found that the X allele and YX genotype in the MBL2 were more frequent in the dengue cases than in the control group. Likewise, the LXPA haplotype was exclusively found in dengue cases, thus probably related to dengue infection in our setting. Moreover, we found a higher frequency of the O allele and AO genotype in the control group. Serum levels of total and functional MBL were higher in dengue naïve infants than in dengue cases. ConclusionsMBL2 variants related to lower production of serum MBL were associated with dengue infection in infants, whereas intermediate to high levels of total and functional serum MBL were associated with protection against dengue infection. These findings highlight the role of MBL2 variants and serum levels of MBL in the susceptibility of children to dengue disease at early ages.

The ambiguous role of mannose-binding lectin (MBL) in human immunity.

Mannose-binding lectin (MBL) and lectin complement pathway have become targets of increasing clinical interest. Many aspects of MBL have been recently explored, including the structural properties that allow it to distinguish self from non-self/altered-self structures. Experimental evidences have declared the additional 5′- and 3′-variants that in amalgamation with well-known secretor polymorphisms change MBL function and concentration. Moreover, the current review highlights the differential behavior of MBL on exposure with extra/intracellular pathogens and in autoimmune diseases, stressing the fact that “high MBL levels can increase diseases susceptibility,” a paradox that needs justification. Attributable to these discrepancies, no absolute level of MBL deficiency could be defined so far and thus must be interpreted for specific diseases through case–control population-specific designs. Overall, it is evident that further research is needed about MBL and the lectin pathway of complement. Particularly, the transformative role of MBL over evolution is of interest and its role with regard to pathogenesis of different diseases and potential therapeutic targets within the respective pathways should be further explored. Apart from this, it is necessary to adopt an extensive locus-wide methodology to apprehend the clinical significance of MBL2 polymorphisms in a variety of infectious diseases by the future studies.

The impact of mannose-binding lectin polymorphisms on lung function in primary ciliary dyskinesia.

Primary ciliary dyskinesia (PCD) is a congenital lung disease that leads to recurrent and chronic lung infection. The resulting inflammation causes lung damage and declines in lung function. Mannose-binding lectin (MBL) is a first line host defense protein of importance for the innate immunity. Polymorphisms in the MBL gene named MBL2 result in unstable and low functional levels MBL proteins. MBL insufficiency is linked to an increased risk of lung infection and to declines in lung function in patients with cystic fibrosis. We investigated whether there is a similar link in patients with PCD. This retrospective longitudinal study included 85 patients with PCD. Diagnostics and age at diagnosis were recorded, complete spirometry data starting at diagnosis, and Pseudomonas aeruginosa infection status over the last 2 years were collected, and the patients were grouped according to MBL2 genotype status (MBL2-sufficient or MBL2-deficient). MBL-deficient patients were diagnosed almost 3 years earlier than MBL-sufficient patients (median 6.1 vs 8.9 years, P < 0.05). There were no differences in the first measured spirometry values, but MBL-deficient patients showed greater declines in forced expiratory volume in one sec (FEV1 ) than patients with MBL sufficiency (z-score: -0.049 per year [95% CI, -0.075; -0.021] vs -0.009 per year [95% CI, -0.033; 0.015]; P = 0.023). No differences were found in forced vital capacity (FVC), FEV1 /FVC, or infection status. MBL-deficiency, which is associated with MBL2 mutations, was associated with a lower age at diagnosis and with steeper declines in FEV1 in patients with PCD. This suggests that the MBL genotype might be a disease modifier in PCD.

Specific contribution of mannose-binding lectin murine isoforms to brain ischemia/reperfusion injury

Mannose-binding lectin (MBL), an initiator of the lectin pathway (LP) of complement activation, is detrimental in ischemic stroke, as shown in clinical studies and rodent models. Whereas humans have one functional MBL protein, rodents have two isoforms, MBL-A and MBL-C, whose functions relative to that of human MBL are unknown. To permit the clinical translation of preclinical data, we aimed to define the specific contributions of MBL-A and MBL-C to brain ischemia. We subjected mice with double (MBL−/−) or single (MBL-A−/− or MBL-C−/−) MBL isoform depletion to transient middle cerebral artery occlusion (tMCAo). MBL−/− mice had fewer neurological deficits and smaller ischemic lesions than WT mice. MBL-A−/− mice had smaller lesions than WT mice and exhibited no significant behavioral defects, whereas MBL-C−/− mice did not differ from WT mice. The induction of Mbl1 and Mbl2 (the MBL-A and MBL-C genes) expression 48 h after tMCAo was similar across genotypes. The time course of Mbl1 and Mbl2 expression in WT ischemic mice showed that Mbl1 activation occurred earlier (24 h) than Mbl2 activation (48 h). The plasma levels of MBL-A and MBL-C in MBL-C−/− and MBL-A−/− mice, respectively, were similar to those in WT mice both at baseline and at 48 h after tMCAo. At 48 h, MBL-A−/− ischemic mice showed higher MBL-C levels in the brain than WT mice. WT and MBL-C−/− ischemic mice had higher LP activity in plasma and, accordingly, higher levels of C3 deposition in the brain than MBL-A−/− and MBL−/− mice. In conclusion, mice with depletion of both MBL isoforms exhibited strong protection from ischemia/reperfusion injury. MBL-A was the main contributor to injury, likely owing to its earlier activation after ischemia and more efficient activation of the complement system than MBL-C.

Association of Mannose-Binding Lectin Gene Polymorphisms with Liver Diseases: A Review

Mannose-Binding Lectin (MBL) is a member of the collectin family and is an important protein in the immune system. It is a pathogen pattern-recognition molecule that binds to specific carbohydrate motifs on the surface of many pathogens. MBL activates complementvialectin pathway. Single nucleotide polymorphisms in the MBL gene influence serum MBL concentration and function. MBL deficiencies increase the risk of infection and disease-specific complications, especially in those who are already immune compromised with pre-existing conditions. This review discusses the molecular genetics of human MBL and the association of MBL polymorphisms with liver diseases including liver fibrosis, viral hepatitis B, viral hepatitis C, and infection post-liver transplantation.

Functional mannose binding lectin levels in patients with pediatric onset systemic lupus erythematosus in remission.

Complement system plays a crucial role in the pathogenesis of systemic lupus erythematosus (SLE). Excessive activation of complement causes tissue injury and SLE occurrence is typically associated with congenital deficiencies of the early components of the classical complement pathway. Mannose-binding lectin (MBL) is recognized as important causative factor in the etio-pathogenesis of SLE and MBL-2 gene has evolved as a candidate gene for SLE susceptibility. This study was done to assess the functional MBL (fMBL) level in SLE patients in remission and its co-relation with disease severity and outcome. Functional MBL levels were compared with age and sex matched healthy controls and were correlated with duration of illness,complement levels and anti-double- stranded DNA antibody levels. Mean fMBL level in patients was found to be 696.19±408.98U/mL and 579.52±393.87U/mL in the control group. Four children had very low fMBL levels (<40U/mL). Functional MBL levels were higher in patients with SLE even when the disease was in remission as compared to healthy controls, although not statistically significant. Large variation exists in fMBL levels in patients with SLE even when in remission. Very low fMBL levels were found in some children with younger age of onset of SLE, multisystem involvement and severe course of the disease. Positive correlation of MBL levels with anti-ds DNA titers suggest that its values vary with activity and could be a potential biomarker of the disease.

Mannose-Binding Lectin (MBL) gene polymorphisms in susceptibility to pulmonary tuberculosis among the Lur population of Lorestan Province of Iran

ObjectiveTuberculosis (TB) is caused by infection of Mycobacterium tuberculosis. Host genetic variability is an important determinant of the risk of developing TB in humans. Although the association between MBL polymorphisms and TB has been studied in various populations, the results are controversial. The aim of this study was to investigate mannose-binding lectin (MBL) gene polymorphisms with susceptibility to pulmonary tuberculosis (PTB) in a Lur population of Iran. MethodsIn this case-control study, four functional MBL gene polymorphisms (HL, XY, PQ and AB) were genotyped by using PCR Single Strand Conformation Polymorphism (SSCP) technique in a Lur population living in Lorestan Province, consisting of 100 patients with pulmonary tuberculosis (PTB) age and sex matched 100 healthy controls (HCs). Association analyses were performed with the SPSS 21 statistical software. ResultsWe found that MBL (HH) genotype polymorphism significantly was associated with increased susceptibility to TB (35% in patients vs. 22% in controls, P=0.0417, OR=1.909, %95 CI=1.020–3.573). Additionally, H allele showed a significant association with increased risk of TB (56.5% in patients vs. 46% in controls, P=0.0357, OR=1.525, %95 CI=1.028–2.262). Also, the distribution of L allele in patients was significantly lower frequency in TB patients compared to controls (43.5% vs. 54%, P=0.0357, OR=0.656, %95 CI=0.442–0.973). However, the allelic and genotypic frequencies of AB, XY and PQ polymorphisms were not significantly different between the patients and the controls. We couldn't detect any significant differences between haplotypes among TB patients and healthy controls. ConclusionsOur findings demonstrated that HH genotype and H allele may increase the susceptibility to pulmonary TB in the Lur population of Iran, although L allele may decrease the susceptibility to pulmonary TB in this population. We suggest that it is necessary to further more studies with larger sample size and other ethnic population.

A comprehensive in silico analysis of non-synonymous and regulatory SNPs of human MBL2 gene.

Mannose binding lectin (MBL) is a liver derived protein which plays an important role in innate immunity. Mannose binding lectin gene 2 (MBL2) polymorphisms are reported to be associated with various diseases. In spite of being exhaustively studied molecule, no attempt has been made till date to comprehensively and systematically analyze the SNPs of MBL2 gene. The present study was carried out to identify and prioritize the SNPs of MBL2 gene for further genotyping and functional studies. To predict the possible impact of SNPs on MBL structure and function SNP data obtained from dbSNP database were analyzed using various bioinformatics tools. Out of total 661 SNPs, only 37 validated SNPs having minor allele frequency ≥0.10 were considered for the present study. These 37 SNPs includes one in 3′ near gene, nine in 3′ UTR, one non-synonymous SNP (nsSNP), thirteen intronic SNPs and thirteen in 5′ near gene. From these 37 SNPs, 11 non-coding SNPs were identified to be of functional significance and evolutionary conserved. Out of these, 4 SNPs from 3′ UTR were found to play role in miRNA binding, 7 SNPs from 5′ near and intronic region were predicted to involve in transcription factor binding and expression of MBL2 gene. One nsSNP Gly54Asp (rs1800450) was found to be deleterious and damaging by both SIFT and Polyphen-2 servers and thus affecting MBL2 protein stability and expression. Protein structural analysis with this amino acid variant was performed by using I-TASSER, RAMPAGE, Swiss-PdbViewer, Chimera and I-mutant. Information regarding solvent accessibility, molecular dynamics and energy minimization calculations showed that this variant causes clashes with neighboring amino acids residues that must interfere in the normal triple helix formation of trimeric subunit and further with the normal assembly of MBL oligomeric form, hence decrease in stability. Thus, findings of the present study indicated 12 SNPs of MBL2 gene to be functionally important. Exploration of these variants may provide novel remedial markers for various diseases.

Mannose-binding lectin gene (MBL2) polymorphisms related to the mannose-binding lectin low levels are associated to dengue disease severity

Dengue is the main arbovirosis in the tropical and subtropical areas of the world. The majority of infected individuals present an asymptomatic outcome while others progress to dengue fever (DF) or dengue haemorrhagic fever (DHF). Dengue infection evolution to severe outcomes is in part, related to innate immunity response. The MBL2 gene encodes for a pathogen recognition pattern molecule, the mannose-binding lectin (MBL). Variant alleles at promoter and structural regions of the MBL2 are related to serum MBL levels and function. Due to the important inflammatory modulation role of MBL, MBL2 polymorphisms could influence dengue progression. Therefore, this study investigated associations of MBL2 polymorphisms and serum MBL levels in patients with dengue. Genotyping of promoter and structural regions of MBL2 was performed by real-time PCR using Taqman® probes in 161 patients presenting DF or DHF outcome. For the serum MBL determination a commercial ELISA kit was used. The variant OO genotype and O allele were associated with DHF (p=0.008 and p=0.009 respectively). Haplotypes correlated to MBL low levels were associated with DHF (p=0.04). Our results support the hypothesis that patients carrying genotypes or haplotypes of low production of MBL would be more susceptible to DHF.

Polymorphisms in the lectin pathway of complement activation influence the incidence of acute rejection and graft outcome after kidney transplantation

There are conflicting data on the role of the lectin pathway of complement activation and its recognition molecules in acute rejection and outcome after transplantation. To help resolve this we analyzed polymorphisms and serum levels of lectin pathway components in 710 consecutive kidney transplant recipients enrolled in the nationwide Swiss Transplant Cohort Study, together with all biopsy-proven rejection episodes and 1-year graft and patient survival. Functional mannose-binding lectin (MBL) levels were determined in serum samples, and previously described MBL2, ficolin 2, and MBL-associated serine protease 2 polymorphisms were genotyped. Low MBL serum levels and deficient MBL2 diplotypes were associated with a higher incidence of acute cellular rejection during the first year, in particular in recipients of deceased-donor kidneys. This association remained significant (hazard ratio 1.75, 95% confidence interval 1.18-2.60) in a Cox regression model after adjustment for relevant covariates. In contrast, there was no significant association with rates of antibody-mediated rejection, patient death, early graft dysfunction or loss. Thus, results in a prospective multicenter contemporary cohort suggest that MBL2 polymorphisms result in low MBL serum levels and are associated with acute cellular rejection after kidney transplantation. Since MBL deficiency is a relatively frequent trait in the normal population, our findings may lead to individual risk stratification and customized immunosuppression.

&amp;lt;i&amp;gt;MBL2&amp;lt;/i&amp;gt; Gene Polymorphism and the Association with Neonatal Sepsis in Egyptian Neonates, a Case Control Study

Mannose binding lectin (MBL) is an important component of innate immunity particularly in neonates whose adaptive immunity is not fully developed. Polymorphism in MBL2 gene promoter and exon1 determines MBL serum level and function. The aim of this study was to investigate the frequency of different MBL2 genotypes in neonatal sepsis among patients of neonatal intensive care unit (NICU). Two hundred and forty-five neonates were enrolled in this study (127 infected and 118 uninfected controls). Multiplex PCR and double amplification refractory mutation system (dARMS) were used for typing of MBL2 exon1 and promoter respectively. Klebsiella species were the most frequently isolated organisms (22.8%). There is no statistical significance difference in the distribution of different expression genotypes between infected group and controls (P = 0.11). However, prevalence of low MBL2 expression genotypes (XA/O and O/O) was higher in infected patients compared to control group (patients 25.2% and controls 15.3%). Low and medium MBL2 expression genotypes were mostly associated with Gram-negative bacterial infections (18.9% and 22.8%) respectively. A statistically significant association of Gram-negative bacterial infections with low MBL2 expression genotypes was found (P = 0.02). Higher frequency of AB and BB genotypes was observed (31.5% and 7.9%) in patients group compared to control, but without statistical significant difference.

The role of mannose binding lectin on fever episodes in pediatric oncology patients.

Despite significant changes in pediatric oncological therapy, mortality is still high, mainly due to infections. Complement system as an ancient immune defense against microorganisms plays a significant role in surmounting infections, therefore, deficiency of its components may have particular importance in malignancies. The present paper assesses the effect of promoter (X/Y) and exon 1 (A/0) polymorphisms of the MBL2 gene altering mannose binding lectin (MBL) serum level in pediatric oncological patients with febrile neutropenia. Furthermore, frequency distribution of MBL2 alleles in children with malignancies and age-matched controls was analysed. Fifty-four oncohematological patients and 53 children who had undergone pediatric surgery were enrolled into this retrospective study. No significant differences were found in the frequency of MBL2 alleles between the hemato-oncologic and control group. The average duration of fever episodes was significantly shorter (p=0.035) in patients carrying genotypes (AY/AY and AY/AX) that encode normal MBL level, compared to individuals with genotypes associated with lower functional MBL level (AX/AX, AY/0, AX/0, or 0/0) (days, median(IQ range) 3.7(0-5.4) vs. 5.0(3.8-6.6), respectively). In conclusion, our data suggest that MBL2 genotypes may influence the course of febrile neutropenia in pediatric patients with malignancies, and may contribute to clarification of the importance of MBL in infections.

Extreme high prevalence of a defective mannose-binding lectin (MBL2) genotype in native South American West Andean populations.

Mannose-binding lectin (MBL) is one of the five recognition molecules in the lectin complement pathway. Common variant alleles in the promoter and structural regions of the human MBL gene (MBL2) influence the stability and serum concentration of the protein. Epidemiological studies have shown that MBL2 variant alleles are associated with susceptibility to and the course of different types of infectious and inflammatory conditions. However, it has been suggested that these alleles are maintained in different populations due to selected advantages for carriers. We investigated the MBL2 allelic variation in indigenous individuals from 12 different West Central South America localities spanning from the desert coast, high altitude Andean plates and the Amazon tropical forest within the territories of Peru (n = 249) (Departments of Loreto, Ucayali, Lambayeque, Junin, Ayacucho, Huancayo and Puno), and Ecuador (n = 182) (Region of Esmeraldas and Santo Domingo de los Colorados). The distribution of MBL2 genotypes among the populations showed that the defective variant LYPB haplotype was very common. It showed the highest frequencies in Puno (Taquile (0.80), Amantani (0.80) and Anapia (0.58) islander communities of the Lake Titicaca), but lower frequencies of 0.22 in Junin (Central Andean highland) and Ucayali (Central Amazonian forest), as well as 0.27 and 0.24 in the Congoma and Cayapa/Chachis populations in the Amazonian forest in Ecuador were also observed. Our results suggest that the high prevalence of the MBL2 LYPB variant causing low levels of functional MBL in serum may mainly reflect a random distribution due to a population bottleneck in the founder populations.

Relation between mannose-binding lectin (MBL) gene codon 54 polymorphism (allele B) and susceptibility to HTLV-1 infection

Mannose-binding lectin (MBL) plays an important role in the innate immune defense against invading microorganisms. Deficiency of functional MBL is linked to polymorphisms in the MBL2 gene. The aim of the study was to determine the influence of MBL2 polymorphisms in susceptibility to HTLV-1 infection. A total of 43 HTLV-1 infected subjects and 127 healthy controls were evaluated for polymorphisms in the coding region of MBL2 gene. The point mutations in exon 1 at codon 54 (allele B) and codon 52 (allele D) and the wild type allele A were detected by PCR-RFLP. The frequency of the allele A, B and D was 66%, 29% and 5% among HTLV-1 infected subjects and 79%, 18% and 3% among healthy controls, respectively. Genotype and allele frequencies were statistically different between both groups, being the allele B more frequent among HTLV-1 infected subjects than in controls (29% and 18%, respectively; p=0.032). Moreover, the homozygous genotype BB was observed in 14% of HTLV-1 patients and only 3% of controls (p=0.016), and it was associated with an almost five-fold higher risk of HTLV-1 infection (p=0.016; OR=4.98, 95%CI=1,33-18,63). Our results suggest that carriers of the MBL2 allele B are more susceptible to HTLV-1 infection. Further studies with a large number of individuals are ongoing to confirm the impact of MBL polymorphisms as genetic determinant of HTLV-1 susceptibility.

Innate immunity in renal transplantation: The role of mannose-binding lectin

Innate immune system plays an important role in the modulation of the inflammatory response during infection and tissue injury/repair. Mannose-binding lectin (MBL) is a component of the innate immune system that activates complement via the lectin pathway. Different polymorphisms of the MBL gene are associated with MBL levels and MBL function. The relationship between MBL and disease is rather complex because MBL behaves as a double-edged sword. In the general population, low serum MBL levels are associated with higher risk of infection, type 2 diabetes, autoimmune and cardiovascular disease. However, in patients with diabetes or autoimmune disease, high MBL levels are associated with more severe renal and cardiovascular comorbidities. In renal transplantation, low MBL serum levels constitute a risk factor for infection, low grade inflammation, new onset diabetes after transplantation and subclinical rejection. Despite these associations suggest that low MBL levels should be associated with poorer renal allograft outcome, epidemiological studies evaluating the predictive value of MBL levels on graft survival are controversial. Taken together, these observations suggest that low MBL serum levels modulate chronic inflammatory response that may influence transplant outcome.

MBL2polymorphisms - manifestations in Bulgarian patients with adult dermatomyositis and systemic lupus erythematosus

Deficiency in some complement factors is known to cause both systemic lupus erythematosus (SLE) and dermatomyositis (DM). Mannose-binding lectin (MBL) is a recognition molecule of the lectin pathway, and its low levels are reported to influence some autoimmune diseases. Furthermore, MBL2 polymorphisms have been described associated with low MBL serum levels due to impaired MBL structure and function. This is a pilot study to investigate the role of MBL2-550G/C (H/L), -221G/C (Y/X), Arg52Cys (D), Gly54Asp (B), Gly57Glu (C) polymorphisms and MBL serum levels as a risk factor for a development of adult DM and SLE in Bulgarian patients. None of the studied MBL2 polymorphisms appeared associated with the diseases investigated. However, we have found an increased OR of MBL2-221XY genotype in the patients with SLE (OR 1.64, 95%CI 0.77-3.52). MBL2 polymorphisms seemed to affect MBL serum levels and to be associated with the clinical features although none of the associations remained statistically significant after Bonferroni correction. The-550L allele showed an association with electromyography findings in patients with DM. The-221XY genotype was associated with photosensitivity in patients with SLE. The 54AB genotype showed an association with malar rash in patients with SLE, but it appeared decreased among SLE patients with ANA. In conclusion, our results suggest that the MBL2 polymorphisms have rather a disease modifying role and they are not associated with the disease susceptibility in adult DM and SLE among Bulgarian patients.

Functional Mannose-Binding Lectin Haplotype Variants are Associated with Alzheimer's Disease

Mannan-Binding lectin (MBL) is a serum lectin and an important constituent of the innate immune system. Processes linked to the innate immune response have previously been implicated in Alzheimer's disease (AD). MBL is associated with blood vessels in the brain and AD patients demonstrate lower MBL levels in the cerebrospinal fluid compared to controls. We investigated six single nucleotide polymorphisms, linked to MBL deficiency, in the corresponding MBL2 gene in AD patients and controls. Two MBL2 haplotypes, LXP and LYQ, were significantly associated with AD risk (OR = 1.6, p = 0.01 and OR = 1.5, p = 0.02, respectively). The present study is the first investigating MBL2 genotypes and haplotypes in relation to AD. Our findings support that the MBL2 gene impact the disease risk.

Chicken mannose-binding lectin (MBL) gene variants with influence on MBL serum concentrations

Mannose-binding lectin (MBL) plays a major role in the innate immune defence by activating the lectin complement pathway or by acting as an opsonin. Two forms of MBL have been characterised from several species, but for humans and chickens, only one form of functional MBL has been described. The human MBL2 gene is highly polymorphic, and it causes varying MBL serum levels. Several of the single-nucleotide polymorphisms (SNPs) have been associated with the severity of diseases of bacterial, viral or parasitic origin. Association between various diseases and different MBL serum levels has also been identified in chickens. In this study, two inbred chicken lines (L10L and L10H) which have been selected for low and high MBL levels in serum and four other experimental chicken lines were analysed for polymorphism in the MBL gene. The presence of polymorphisms in the MBL gene was revealed by southern blot analyses, and the differences in the serum concentrations of MBL were found to be of transcriptional origin according to real-time quantitative reverse transcription PCR analysis. Several SNPs were discovered in the promoter and the 5' untranslated region of the chicken MBL gene which resulted in the identification of six different alleles. Mapping of regulatory elements in the promoter region was performed, and SNPs that could affect the MBL serum concentration were identified. One SNP that was found to be located in a TATA box was altered in one of the six alleles only. This allele was associated with low MBL serum concentration.