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The Epidemiology of Recurrent Pregnancy Loss
Published in Howard J.A. Carp, Recurrent Pregnancy Loss, 2020
A series of factors associated with RPL—aPL, hereditary thrombophilias, and MBL deficiency—have also been associated with late miscarriage, low birthweight, and perinatal complications [57,59]. Since RPL per se seems to be associated with perinatal complications and low birthweight, prospective studies of the effect of the mentioned factors on perinatal complications should be adjusted for the confounding effect of the number and type of previous miscarriages.
Importance of mannose-binding lectin2 polymorphism (rs1800450) in infections in children
Published in Biomarkers, 2022
Metin Uysalol, Suheyla Gumus, Raif Yildiz, Ezgi Pasli Uysalol, Sacide Pehlivan, Mustafa Pehlivan, Istemi Serin
Literature data and our results reveal bacterial infections and MBL deficiency. Bacterial infections such as Streptococcus pneumonia (Roy et al.2002, Eisen et al.2008), legionella (Kuipers et al.2003, Eisen et al.2007, Herpers et al.2007), mycoplasma (Hamvas et al.2005), and MBL have been demonstrated in many past studies. The relationship between MBL deficiency, low MBL expression associated genotypes, and pneumonia has been clearly demonstrated. Viral infections contain unclear data. In a study on the respiratory syncytial virus (RSV), low MBL levels were shown to be associated with severe RSV infection (Ribeiro et al.2008). Although there are many data showing that MBL can inactivate the influenza virus (Anders et al.1990), there are no clinical studies showing that there is a clear relationship between MBL influenza. In this context, the observation of higher MBL-associated genotypes in our bronchiolitis cases compared to healthy controls constitutes an important contribution point in terms of the literature.
Mannose-Binding Lectin Levels in Late-Onset Sepsis in Preterm Infants: Results from a Prospective Study in a Tertiary Care Center
Published in Fetal and Pediatric Pathology, 2020
Pelin Dogan, Hilal Ozkan, Nilgun Koksal, Haluk Barbaros Oral, Solmaz Celebi, Onur Bagci, Ipek Guney Varal
Mannose-binding lectin (MBL) is a member of the collectin family that enables the lectin pathway of the complement system, and it has an important role in binding to several microorganisms. Common polymorphisms occur at the MBL2 locus, leading to decreased circulating MBL levels. MBL deficiency is observed in approximately one-third of the population. Low MBL levels are associated with increased infection rates in preterm infants [5]. The adaptive host response to infection in preterm infants is damaged for miscellaneous reasons. The absence of passively derived maternal antibodies, decreased function of neutrophils and suboptimal functioning of the acquired immune system might be liable for the host-defence disruptions in infants; hence, newborns have increased sensitivity to infections [6]. MBL is considered an important part of the innate immune system, and its deficiency may be a risk factor for infection in this patient category [7, 8].
Systemic lupus erythematosus and immunodeficiency
Published in Immunological Medicine, 2019
Tetsuji Sawada, Daiki Fujimori, Yusuke Yamamoto
As with the components of the complement system, several studies have suggested an association between MBL deficiency and increased susceptibility to infection and development of SLE. The most frequent cause of MBL deficiency is a genetic mutation that causes substitution of an amino acid at position 54 in Asians and Caucasians and at position 57 in Africans, leading to alteration in the structure of the protein in a way that induces instability and subsequently enhances degradation of MBL in homozygous individuals (approximately 5–10% in all races). MBL deficiency has not been shown to be associated with susceptibility to infection in healthy individuals but was shown to be a significant risk factor for severe bacterial infection in immunocompromised hosts, such as children, patients with human immunodeficiency virus infection, and patients undergoing hematopoietic stem cell transplantation [40].