Mannan‐Binding Lectin Deficiency is Associated with Unexplained Recurrent Miscarriage

Christiansen, Thomas; Kilpatrick,; Souter, Vivienne L.; Varming,; Thiel, Steffen; Jensenius,

doi:10.1046/j.1365-3083.1999.00473.x

Cited by 98 publications

(52 citation statements)

References 12 publications

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“…More detailed analysis of the MBL gene revealed seven distinct MBL haplotypes in humans, four of which (LYPB, LYQC, HYPD, and LXPA) dictate low serum levels (45,47). MBL deficiency, defined as Ͻ100 ng of MBL per millileter in plasma, is very common in some ethnicities from 15% of the Caucasian population to as high as 30% in certain African populations (45,(47)(48)(49)(50). Compelling clinical studies have suggested that MBL deficiency was associated with severe infections following chemotherapy, postoperative, and after stem cell transplantations (51)(52)(53)(54)(55).…”

Section: Discussionmentioning

confidence: 99%

Deficiency of Mannose-Binding Lectin Greatly Increases Susceptibility to Postburn Infection withPseudomonas aeruginosa

Møller-Kristensen

Ip²,

Shi³

et al. 2006

The Journal of Immunology

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Burn injury disrupts the mechanical and biological barrier that the skin presents against infection by symbionts like the Pseudomonas aeruginosa, a Gram-negative bacteria. A combination of local factors, antimicrobial peptides, and resident effector cells form the initial response to mechanical injury of the skin. This activity is followed by an inflammatory response that includes influx of phagocytes and serum factors, such as complement and mannose-binding lectin (MBL), which is a broad-spectrum pattern recognition molecule that plays a key role in innate immunity. A growing consensus from studies in humans and mice suggests that lack of MBL together with other comorbid factors predisposes the host to infection. In this study we examined whether MBL deficiency increases the risk of P. aeruginosa infection in a burned host. We found that both wild-type and MBL null mice were resistant to a 5% total body surface area burn alone or s.c. infection with P. aeruginosa alone. However, when mice were burned then inoculated s.c. with P. aeruginosa at the burn site, all MBL null mice died by 42 h from septicemia, whereas only one-third of wild-type mice succumbed (p = 0.0005). This result indicates that MBL plays a key role in containing and preventing a systemic spread of P. aeruginosa infection following burn injury and suggests that MBL deficiency in humans maybe a premorbid variable in the predisposition to infection in burn victims.

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Section: Discussionmentioning

confidence: 99%

Deficiency of Mannose-Binding Lectin Greatly Increases Susceptibility to Postburn Infection withPseudomonas aeruginosa

Møller-Kristensen

Ip²,

Shi³

et al. 2006

The Journal of Immunology

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“…The samples were added to the wells, and bound H-ficolin was detected as above. Inhibition of MBL binding was tested in the same manner on the mannan-coated wells, and bound MBL was quantified using europium-labeled monoclonal anti-MBL antibodies as described previously (38,39). (24) as well as recombinant M-ficolin (produced in CHO cells and kindly provided by Anne Trommelholt Jepsen, University of Southern Denmark, Denmark) were added to the wells in 100 l of TBS/ tw/Ca 2ϩ and incubated overnight at 4°C.…”

Section: Trifma For H-ficolin Binding To a Viridians And Acbsa-mentioning

confidence: 99%

Studies of the Pattern Recognition Molecule H-ficolin

Zacho

Jensen

Terp

et al. 2012

Journal of Biological Chemistry

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Background: H-ficolin is a pattern recognition molecule of the human innate immune system. Results: The ligand specificity of H-ficolin is explored, and a purification procedure is developed. Conclusion: H-ficolin binds to patterns of acetyl groups and activates complement upon binding. Significance: The findings expand and emphasize the differences of the specificities of the three human ficolins (H-, L-, and M-ficolin).

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“…An ELISA of mannan-binding activity was used to detect functional oligomers of the MBL protein in serum. 30 The assay was performed in the Department of Microbiology and Immunology, University of Melbourne, without reference to the participant's genotype. Rabbit antihuman MBL serum was obtained from Drs Kazue Takahashi and Alan Ezekowitz, Department of Pediatrics, Massachusetts General Hospital, Boston, USA.…”

Section: Serum Mblmentioning

confidence: 99%

Mannose-binding lectin gene polymorphism predicts hospital admissions for COPD infections

et al. 2003

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Infection frequently causes exacerbations of chronic obstructive pulmonary disease (COPD). Mannose-binding lectin (MBL) is a pattern-recognition receptor that assists in clearing microorganisms. Polymorphisms in the MBL2 gene reduce serum MBL levels and are associated with risk of infection. We studied whether the MBL2 codon 54 B allele affected serum MBL levels, admissions for infective exacerbation in COPD and disease susceptibility. Polymorphism frequency was determined by PCR-RFLP in 200 COPD patients and 104 smokers with normal lung function. Serum MBL was measured as mannan-binding activity in a subgroup of 82 stable COPD patients. Frequency of COPD admissions for infective exacerbation was ascertained for a 2-year period. The MBL2 codon 54 B allele reduced serum MBL in COPD patients. In keeping, patients carrying the low MBL-producing B allele had increased risk of admission for infective exacerbation (OR 4.9, P corrected ¼ 0.011). No association of MBL2 genotype with susceptibility to COPD was detected. In COPD, serum MBL is regulated by polymorphism at codon 54 in its encoding gene. Low MBL-producing genotypes were associated with more frequent admissions to hospital with respiratory infection, suggesting that the MBL2 gene is disease-modifying in COPD. MBL2 genotype should be explored prospectively as a prognostic marker for infection risk in COPD.

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Mannan‐Binding Lectin Deficiency is Associated with Unexplained Recurrent Miscarriage

Cited by 98 publications

References 12 publications

Deficiency of Mannose-Binding Lectin Greatly Increases Susceptibility to Postburn Infection withPseudomonas aeruginosa

Deficiency of Mannose-Binding Lectin Greatly Increases Susceptibility to Postburn Infection withPseudomonas aeruginosa

Studies of the Pattern Recognition Molecule H-ficolin

Mannose-binding lectin gene polymorphism predicts hospital admissions for COPD infections

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