L-ficolin in children with recurrent respiratory infections

Atkinson, Anne; Cedzyński, Maciej; Szemraj, Janusz; Świerzko, Anna St.; Bąk‐Romaniszyn, Leokadia; Banasik, Mirosław; Zeman, Krzysztof; Matsushita, Misao; Turner, Marc; Kilpatrick, David C.

doi:10.1111/j.1365-2249.2004.02634.x

Cited by 66 publications

(51 citation statements)

References 21 publications

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“…In a cohort of Polish children with recurrent respiratory tract infection, a group of patients with underlying atopic disorder were significantly more likely to have L-ficolin levels less than the lower range seen in healthy controls. The same did not apply to the group of children with recurrent infection but no other detectable laboratory abnormalities [77] . No association between FCN2 polymorphisms and disease susceptibility [78] was found in the UK invasive pneumococcal disease cohort previously studied for MBL deficiency association [2] .…”

Section: Molecular and Clinical Comparisons Between Ficolins And Mblmentioning

confidence: 94%

Mannose-Binding Lectin Deficiency and Respiratory Tract Infection

Eisen¹

2009

J Innate Immun

119

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Mannose-binding lectin (MBL) is an innate immune system pattern recognition protein that kills a wide range of pathogenic microbes through complement activation. A substantial proportion of all human populations studied to date have MBL deficiency due to MBL2 polymorphisms, which potentially increases susceptibility to infectious disease. MBL binds numerous respiratory pathogens but the capsule of Streptococcus pneumoniae abrogates its efficient binding. Clinical studies in humans have shown that MBL deficiency appears to predispose to severe respiratory tract infection. A recent meta-analysis shows that MBL deficiency was associated with death in patients with pneumococcal infection after adjusting for bacteraemia and comorbidities. Human clinical studies have also shown associations between MBL deficiency and various less common respiratory infections. Intracellular infections like tuberculosis may be less common with MBL deficiency because of reduced opsonophagocytosis. Lung secretions contain small amounts of MBL that are potentially sufficient to activate complement, but their measurement is confounded by dilution inherent in collection techniques. Therefore, if this protein does play a role in pulmonary immunity it is presumably through prevention of haematogenous dissemination of respiratory pathogens while adding to mucosal defences. Ficolins are collectins that are structurally and functionally related to MBL and are either present in serum or expressed in tissues including the lung. Limited variation in serum levels of L- and H-ficolin result from the presence of FCN2 and FCN3 polymorphisms. Initial studies on the impact of FCN2 polymorphisms or low L-ficolin levels do not seem to show major associations with respiratory infection. MBL is being developed as a new immunotherapeutic agent for prevention of infection in immunocompromised hosts. The available literature suggests that it may also be of benefit in MBL deficient patients with severe pneumonia. This review concentrates on clinical associations between MBL deficiency and susceptibility to respiratory tract infection.

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Section: Molecular and Clinical Comparisons Between Ficolins And Mblmentioning

confidence: 94%

Mannose-Binding Lectin Deficiency and Respiratory Tract Infection

Eisen¹

2009

J Innate Immun

119

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“…In recent years, the association between genetic variations in MBL2 , and to a lesser extent FCN2 , and susceptibility to disease have been the subject of various studies 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31. An association between MBL2 polymorphisms and clinical outcome has been described in children with recurrent infections22 and in adult patients with meningococcal sepsis 17…”

Section: Introductionmentioning

confidence: 99%

“…An association between MBL2 polymorphisms and clinical outcome has been described in children with recurrent infections22 and in adult patients with meningococcal sepsis 1729 Behçet's disease,20 peritonitis in patients undergoing peritoneal dialysis28 and recurrent respiratory infections in children 16, 18. More recently, the role of MBL2 polymorphisms in invasive pneumococcal disease25, 27, 30, 31 and CAP23, 24 has been studied but with conflicting results.…”

Section: Introductionmentioning

confidence: 99%

Mannose‐binding lectin and l‐ficolin polymorphisms in patients with community‐acquired pneumonia caused by intracellular pathogens

et al. 2017

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SummaryCommunity‐acquired pneumonia (CAP) is the leading infectious disease requiring hospitalization in the western world. Genetic variability affecting the host response to infection may play a role in susceptibility and outcome in patients with CAP. Mannose‐binding lectin (MBL) and l‐ficolin (l‐FCN) are two important activators of the complement system and they can enhance phagocytosis by opsonization. In a prospective cohort of 505 Dutch patients with CAP and 227 control participants we studied whether polymorphisms in the MBL (MBL2) and FCN (FCN2) genes influenced susceptibility and outcome. No difference in frequency of these genotypes was found between patients with CAP in general and controls. However, the +6424G>T single nucleotide polymorphism (SNP) in FCN2 was more common in patients with a Coxiella burnetii pneumonia (P = 0·014). Moreover, the haplotypes coding for the highest MBL serum levels (YA/YA and YA/XA) predisposed to atypical pneumonia (C. burnetii, Legionella or Chlamydia species or Mycoplasma pneumoniae) compared with controls (P = 0·016). Furthermore, patients with these haplotypes were more often bacteraemic (P = 0·019). It can therefore be concluded that MBL2 and FCN2 polymorphisms are not major risk factors for CAP in general, but that the +6424G>T SNP in the FCN2 gene predisposes to C. burnetii pneumonia. In addition, patients with genotypes corresponding with high serum MBL levels are at risk for atypical pneumonia, possibly caused by enhanced phagocytosis, thereby promoting cell entry of these intracellular bacteria.

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“…A few recent studies have revealed that a low concentration of L-ficolin correlated with recurrent respiratory infections in childhood [131], but there is no data regarding the serum concentrations of L-ficolin in maintenance HD patients. In collaboration with Inoshita et al [132], we performed a study on complement deficiencies screened by measurement of functional activities of the three complement pathways in HD patients.…”

Section: Peritoneal Dialysis: Animal Model and Patientsmentioning

confidence: 99%

Pathogenesis and Treatment of Chronic Kidney Disease: A Review of Our Recent Basic and Clinical Data

Tomino

2014

Kidney Blood Press Res

439

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Chronic kidney disease (CKD) is a worldwide public health problem that affects millions of people from all racial and ethnic groups. At end of 2013, over 300,000 Japanese patients had maintenance dialysis therapy (JSDT). In Japan, the major causes of end stage kidney disease (ESKD) are chronic glomerulonephritis (particularly IgA nephropathy), type 2 diabetic nephropathy, and hypertensive nephrosclerosis. Hypertension is a major factor driving the progression of CKD to ESKD. Since many features of the pathogenesis of IgA nephropathy are still obscure, specific treatment is not yet available. However, efforts by investigators around the world have gradually clarified different aspects of the pathogenesis and treatment of IgA nephropathy. Today, around half of all diabetic patients in Japan receive medical treatment. Type 2 diabetic nephropathy is one of the major long-term microvascular complications occurring in nearly 40% of Japanese diabetic patients. The pathogenesis of diabetic nephropathy involves both genetic and environmental factors. However, the candidate genes related to the initiation and progression of the disorder are still obscure in patients with diabetic nephropathy. Regarding environmental factors, the toxicity of persistent hyperglycemia, reactive oxygen species, systemic and/or glomerular hypertension, dyslipidemia and complement are considered to play an important role. The first part of this review covers the pathogenesis of IgA nephropathy and type 2 diabetic nephropathy, and combines the clinicopathological findings in patients with our research on the ddY and KKA-y mouse models (spontaneous animal models for IgA nephropathy and diabetic nephropathy, respectively). In Japan, the major renal replacement therapies (RRT) are peritoneal dialysis (PD) and hemodialysis (HD). The second part of this review focuses on PD and HD. Based on our research findings from patients and as well as from animal models, we discuss strategies for the management of patients on PD and HD. i 2015 S. Karger AG, Basel

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L-ficolin in children with recurrent respiratory infections

Cited by 66 publications

References 21 publications

Mannose-Binding Lectin Deficiency and Respiratory Tract Infection

Mannose-Binding Lectin Deficiency and Respiratory Tract Infection

Mannose‐binding lectin and l‐ficolin polymorphisms in patients with community‐acquired pneumonia caused by intracellular pathogens

Pathogenesis and Treatment of Chronic Kidney Disease: A Review of Our Recent Basic and Clinical Data

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