Mannose-binding lectin (MBL) is an innate immune system pattern recognition molecule that kills a wide range of pathogens via the lectin complement pathway. MBL deficiency is associated with severe infection but the best measure of this deficiency is undecided. We investigated the influence of MBL functional deficiency on the development of sepsis in 195 adult patients, 166 of whom had bloodstream infection and 35 had pneumonia. Results were compared with 236 blood donor controls. MBL function (C4b deposition) and levels were measured by enzyme-linked immunosorbent assay. Using receiver-operator characteristics of MBL function in healthy controls, we identified a level of <0.2 U microL(-1) as a highly discriminative marker of low MBL2 genotypes. Median MBL function was lower in sepsis patients (0.18 U microL(-1)) than in controls (0.48 U microL(-1), P<0.001). MBL functional deficiency was more common in sepsis patients than controls (P<0.001). MBL functional deficient patients had significantly higher sequential organ failure assessment (SOFA) scores and higher MBL function and levels were found in patients with SOFA scores predictive of good outcome. Deficiency of MBL function appears to be associated with bloodstream infection and the development of septic shock. High MBL levels may be protective against severe sepsis.

Download full-text PDF

Source
http://dx.doi.org/10.1111/j.1574-695X.2006.00144.xDOI Listing

Publication Analysis

Top Keywords

mannose-binding lectin
8
adult patients
8
mbl function
8
mbl
5
low mannose-binding
4
lectin function
4
function associated
4
associated sepsis
4
sepsis adult
4
patients mannose-binding
4

Similar Publications

The innate immune system plays a critical role in the rapid recognition and elimination of pathogens through pattern recognition receptors (PRRs). Among these PRRs are the C-type lectins (CTLs) langerin, mannan-binding lectin (MBL), and surfactant protein D (SP-D), which recognize carbohydrate patterns on pathogens. Each represents proteins from different compartments of the body and employs separate effector mechanisms.

View Article and Find Full Text PDF

Sickle Cell Anemia and Inflammation: A Review of Stones and Landmarks Paving the Road in the Last 25 Years.

Hematol Rep

January 2025

Laboratory of Immunobiology and Immunogenetics, Post Graduation Program in Genetics and Molecular Biology (PPGBM), Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre 91501-970, Brazil.

A quarter of a century ago, sickle cell disease (SCD) was mainly viewed as a typical genetic disease inherited as a classical Mendelian trait. Therefore, the main focus concerning SCD was on diagnosis, meaning, genotyping, and identification of homozygous and heterozygous individuals carrying the relevant HbS mutant allele. Nowadays, it is well established that sickle cell disease is indeed the result of homozygosis for the HbS variant, although this single feature is not capable of explaining the highly diverse clinical presentation of SCD.

View Article and Find Full Text PDF

Probing the interaction of mannose-binding lectin with healthy and sickle cell anemia red blood cells and its role in cellular biomechanics.

Int J Biol Macromol

January 2025

Departmento de Biofísica e Radiobiologia, Universidade Federal de Pernambuco, Recife, Pernambuco 50670-901, Brazil. Electronic address:

Mannose-binding lectin (MBL) is an important glycoprotein of the human innate immune system. Furthermore, individuals with sickle cell anemia (SCA) and MBL deficiency seem more susceptible to vaso-occlusive crises, suggesting an MBL role on HbSS red blood cells (RBCs). This study investigated the interaction of MBL with HbA (healthy) and HbSS RBCs using optical tweezers (OT) and atomic force microscopy (AFM).

View Article and Find Full Text PDF

Aflatoxin B1 (AFB1) has been reported to synergize with hepatitis B virus (HBV) to induce development of hepatocellular carcinoma (HCC). Precise daily exposure to AFB1 and its contribution to liver injury have not been quantified and have even been disregarded due to lack of convenient detection, and the strong species specificity of HBV infection has restricted research on their synergistic harm. Hence, our objective was to investigate the molecular mechanisms by which AFB1 exacerbates HBV-related injury.

View Article and Find Full Text PDF

Macrophage-specific in vivo RNA editing promotes phagocytosis and antitumor immunity in mice.

Sci Transl Med

January 2025

College of Pharmaceutical Sciences, State Key Laboratory of Advanced Drug Delivery and Release Systems, Zhejiang University, Hangzhou 310058, China.

Macrophages play a central role in antitumor immunity, making them an attractive target for gene therapy strategies. However, macrophages are difficult to transfect because of nucleic acid sensors that can trigger the degradation of foreign plasmid DNA. Here, we developed a macrophage-specific editing (MAGE) system by which compact plasmid DNA encoding a CasRx editor can be delivered to macrophages by a poly(β-amino ester) (PBAE) carrier to bypass the DNA sensor and enable RNA editing in vitro and in vivo.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!