Assignment of the Human Pulmonary Surfactant Protein D Gene (SFTP4) to 10q22-q23 Close to the Surfactant Protein A Gene Cluster

Kölble, Konrad; Lu, Jinhua; Mole, Sara; Kaluz, Štefan; Reid, Kenneth B.M.

doi:10.1006/geno.1993.1324

Cited by 57 publications

(34 citation statements)

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“…18pter-p11.3) and other collectin genes (chr. 10q11.2-q23.1) (2,15,26). These findings suggest that CL-K1 and CL-L1 may have been formed via similar process of molecular evolution which are different from the other collectin genes.…”

Section: Discussionmentioning

confidence: 95%

Identification and Characterization of a Novel Human Collectin CL‐K1

Keshi

Sakamoto

Kawai

et al. 2006

Microbiology and Immunology

122

183

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Collectins are a family of C‐type lectins with two characteristic structures, collagen like domains and carbohydrate recognition domains. They recognize carbohydrate antigens on microorganisms and act as host‐defense. Here we report the cloning and characterization of a novel collectin CL‐K1. RT‐PCR analyses showed CL‐K1 mRNA is present in all organs. The deduced amino acid sequence and the data from immunostaining of CL‐K1 cDNA expressing CHO cells revealed that CL‐K1 is expressed as a secreted protein. CL‐K1 is found in blood by immunoblotting and partial amino acid analyses. CL‐K1 showed Ca2+‐dependent sugar binding activity of fucose and weakly mannose but not N‐acetyl‐galactosamine, N‐acetyl‐glucosamine, or maltose, though mannose‐binding lectin (MBL) containing similar amino acid motif. CL‐K1 can recognize specially several bacterial saccharides due to specific sugar‐binding character. Elucidation of the role of two ancestor collectins of CL‐K1 and CL‐L1 could lead to see the biological function of collectin family.

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Section: Discussionmentioning

confidence: 95%

Identification and Characterization of a Novel Human Collectin CL‐K1

Keshi

Sakamoto

Kawai

et al. 2006

Microbiology and Immunology

122

183

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“…The location of the MBL2 gene lies close to the SP-A and SP-D loci on chromosome 10q [79] . Potentially, some of the associations recorded above between MBL2 polymorphism and lower respiratory tract infection are reflective of associated variation in the surfactant protein genes.…”

Section: Unresolved Issues In Mbl's Role In Susceptibility To Respiramentioning

confidence: 99%

Mannose-Binding Lectin Deficiency and Respiratory Tract Infection

Eisen¹

2009

J Innate Immun

118

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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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“…Human SP-A and SP-D genes are located on the chromosome 10q22-q23 (Kölble et al 1993). SP-A consists of one SP-A1 and two SP-A2 molecules forming a trimer (Karinch et al 1997).…”

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confidence: 99%

Polymorphisms in the Surfactant Protein A Gene Are Associated with the Susceptibility to Recurrent Urinary Tract Infection in Chinese Women

Liu

Liang

et al. 2010

Tohoku J. Exp. Med.

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Recurrent urinary tract infection (r-UTI) remains one of the common infections affecting adult female. Almost 27% of women developed a recurrent UTI within the 6 months (Foxman 1990) and nearly 50% of women developed a recurrence within the first year following the initial infection (Mabeck 1972). Clinical studies showed that only a fraction of r-UTI patients had obvious functional, anatomic and behavioral risk factors, which were considered to be strongly associated with an increased risk of r-UTI. Recently, genetic studies have reported the associations of polymorphisms within innate immune molecules such as Toll-like receptor 2 and 4 (TLR2 and TLR4) with r

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Assignment of the Human Pulmonary Surfactant Protein D Gene (SFTP4) to 10q22-q23 Close to the Surfactant Protein A Gene Cluster

Cited by 57 publications

References 0 publications

Identification and Characterization of a Novel Human Collectin CL‐K1

Identification and Characterization of a Novel Human Collectin CL‐K1

Mannose-Binding Lectin Deficiency and Respiratory Tract Infection

Polymorphisms in the Surfactant Protein A Gene Are Associated with the Susceptibility to Recurrent Urinary Tract Infection in Chinese Women

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