Mannose-binding Lectin (MBL) as a susceptible host factor influencing Indian Visceral Leishmaniasis

Abstract Visceral Leishmaniasis (VL), caused by Leishmania donovani is endemic in the Indian sub-continent. Mannose-binding Lectin (MBL) is a complement lectin protein that binds to the surface of Leishmania promastigotes and results in activation of the complement lectin cascade. We utilized sample...

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Veröffentlicht in:Parasitology international 2015-12, Vol.64 (6), p.591-596
Hauptverfasser: Mishra, Anshuman, Antony, Justin S, Gai, Prabhanjan, Sundaravadivel, Pandarisamy, Hoang van, Tong, Jha, Aditya Nath, Singh, Lalji, Velavan, Thirumalaisamy P, Thangaraj, Kumarasamy
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container_issue 6
container_start_page 591
container_title Parasitology international
container_volume 64
creator Mishra, Anshuman
Antony, Justin S
Gai, Prabhanjan
Sundaravadivel, Pandarisamy
Hoang van, Tong
Jha, Aditya Nath
Singh, Lalji
Velavan, Thirumalaisamy P
Thangaraj, Kumarasamy
description Abstract Visceral Leishmaniasis (VL), caused by Leishmania donovani is endemic in the Indian sub-continent. Mannose-binding Lectin (MBL) is a complement lectin protein that binds to the surface of Leishmania promastigotes and results in activation of the complement lectin cascade. We utilized samples of 218 VL patients and 215 healthy controls from an Indian population. MBL2 functional variants were genotyped and the circulating MBL serum levels were measured. MBL serum levels were elevated in patients compared to the healthy controls (adjusted P = 0.007). The MBL 2 promoter variants − 78C/T and + 4P/Q were significantly associated with relative protection to VL (− 78C/T, OR = 0.7, 95% CI = 0.5–0.96, adjusted P = 0.026 and + 4P/Q, OR = 0.66, 95% CI = 0.48–0.9, adjusted P = 0.012). MBL2 * LYQA haplotypes occurred frequently among controls (OR = 0.69, 95% CI = 0.5–0.97, adjusted P = 0.034). MBL recognizes Leishmania and plays a relative role in establishing L. donovani infection and subsequent disease progression. In conclusion, MBL2 functional variants were associated with VL.
doi_str_mv 10.1016/j.parint.2015.08.003
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Mannose-binding Lectin (MBL) is a complement lectin protein that binds to the surface of Leishmania promastigotes and results in activation of the complement lectin cascade. We utilized samples of 218 VL patients and 215 healthy controls from an Indian population. MBL2 functional variants were genotyped and the circulating MBL serum levels were measured. MBL serum levels were elevated in patients compared to the healthy controls (adjusted P = 0.007). The MBL 2 promoter variants − 78C/T and + 4P/Q were significantly associated with relative protection to VL (− 78C/T, OR = 0.7, 95% CI = 0.5–0.96, adjusted P = 0.026 and + 4P/Q, OR = 0.66, 95% CI = 0.48–0.9, adjusted P = 0.012). MBL2 * LYQA haplotypes occurred frequently among controls (OR = 0.69, 95% CI = 0.5–0.97, adjusted P = 0.034). MBL recognizes Leishmania and plays a relative role in establishing L. donovani infection and subsequent disease progression. 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Mannose-binding Lectin (MBL) is a complement lectin protein that binds to the surface of Leishmania promastigotes and results in activation of the complement lectin cascade. We utilized samples of 218 VL patients and 215 healthy controls from an Indian population. MBL2 functional variants were genotyped and the circulating MBL serum levels were measured. MBL serum levels were elevated in patients compared to the healthy controls (adjusted P = 0.007). The MBL 2 promoter variants − 78C/T and + 4P/Q were significantly associated with relative protection to VL (− 78C/T, OR = 0.7, 95% CI = 0.5–0.96, adjusted P = 0.026 and + 4P/Q, OR = 0.66, 95% CI = 0.48–0.9, adjusted P = 0.012). MBL2 * LYQA haplotypes occurred frequently among controls (OR = 0.69, 95% CI = 0.5–0.97, adjusted P = 0.034). MBL recognizes Leishmania and plays a relative role in establishing L. donovani infection and subsequent disease progression. In conclusion, MBL2 functional variants were associated with VL.</description><subject>Case-Control Studies</subject><subject>Complement System Proteins - immunology</subject><subject>Cross-Sectional Studies</subject><subject>Female</subject><subject>Gastroenterology and Hepatology</subject><subject>Gene Frequency - genetics</subject><subject>Genotype</subject><subject>Humans</subject><subject>India</subject><subject>Infectious Disease</subject><subject>Leishmania donovani</subject><subject>Leishmania donovani - immunology</subject><subject>Leishmaniasis, Visceral - immunology</subject><subject>Leishmaniasis, Visceral - parasitology</subject><subject>Leishmaniasis, Visceral - pathology</subject><subject>Male</subject><subject>Mannose-Binding Lectin - blood</subject><subject>Mannose-Binding Lectin - genetics</subject><subject>Mannose-Binding Lectin - metabolism</subject><subject>MBL serum level</subject><subject>MBL2</subject><subject>Polymorphism, Single Nucleotide - genetics</subject><subject>Promoter Regions, Genetic - genetics</subject><subject>Visceral Leishmaniasis</subject><issn>1383-5769</issn><issn>1873-0329</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUtP3DAURi3Uimf_Aaq8hEVSPxI_NpUKKi3SIBbQqjvLdpziacYZfBMk_n0dDXTRDSt7cb7v2ucidEpJTQkVn9b11uaYppoR2tZE1YTwPXRIleQV4Uy_K3eueNVKoQ_QEcCaFFBKuo8OmGBaMk0Okb-xKY0QKhdTF9NvvAp-igmf3VyszrEFbDHM4MN2im4I-GGECffWT2PGMfXDHJJfUtclbBP-GQua7VBaIjxsbIoWIpyg970dIHx4OY_Rj6uv95ffq9Xtt-vLL6vKNw2dqpapnjmmBGuVEz2TvrXWWa-0pCx43inhnRVeyZY5rYRW3jPJSaOZdEo3_Bid7Xq3eXycA0xms7xnGGwK4wyGSio0L350QZsd6vMIkENvtjlubH42lJhFr1mbnV6z6DVEmaK3xD6-TJjdJnT_Qq8-C_B5B4Tyz6cYsgEfi6PQxVzEmm6Mb034v8APMUVvhz_hOcB6nHMqDg01wAwxd8uKlw3TtmyXt7_4X7Irojo</recordid><startdate>20151201</startdate><enddate>20151201</enddate><creator>Mishra, Anshuman</creator><creator>Antony, Justin S</creator><creator>Gai, Prabhanjan</creator><creator>Sundaravadivel, Pandarisamy</creator><creator>Hoang van, Tong</creator><creator>Jha, Aditya Nath</creator><creator>Singh, Lalji</creator><creator>Velavan, Thirumalaisamy P</creator><creator>Thangaraj, Kumarasamy</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20151201</creationdate><title>Mannose-binding Lectin (MBL) as a susceptible host factor influencing Indian Visceral Leishmaniasis</title><author>Mishra, Anshuman ; Antony, Justin S ; Gai, Prabhanjan ; Sundaravadivel, Pandarisamy ; Hoang van, Tong ; Jha, Aditya Nath ; Singh, Lalji ; Velavan, Thirumalaisamy P ; Thangaraj, Kumarasamy</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c441t-528f2b286258b6f27c5aabac89712ec3d86cba6c8752b98698cc27304927b8943</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Case-Control Studies</topic><topic>Complement System Proteins - immunology</topic><topic>Cross-Sectional Studies</topic><topic>Female</topic><topic>Gastroenterology and Hepatology</topic><topic>Gene Frequency - genetics</topic><topic>Genotype</topic><topic>Humans</topic><topic>India</topic><topic>Infectious Disease</topic><topic>Leishmania donovani</topic><topic>Leishmania donovani - immunology</topic><topic>Leishmaniasis, Visceral - immunology</topic><topic>Leishmaniasis, Visceral - parasitology</topic><topic>Leishmaniasis, Visceral - pathology</topic><topic>Male</topic><topic>Mannose-Binding Lectin - blood</topic><topic>Mannose-Binding Lectin - genetics</topic><topic>Mannose-Binding Lectin - metabolism</topic><topic>MBL serum level</topic><topic>MBL2</topic><topic>Polymorphism, Single Nucleotide - genetics</topic><topic>Promoter Regions, Genetic - genetics</topic><topic>Visceral Leishmaniasis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mishra, Anshuman</creatorcontrib><creatorcontrib>Antony, Justin S</creatorcontrib><creatorcontrib>Gai, Prabhanjan</creatorcontrib><creatorcontrib>Sundaravadivel, Pandarisamy</creatorcontrib><creatorcontrib>Hoang van, Tong</creatorcontrib><creatorcontrib>Jha, Aditya Nath</creatorcontrib><creatorcontrib>Singh, Lalji</creatorcontrib><creatorcontrib>Velavan, Thirumalaisamy P</creatorcontrib><creatorcontrib>Thangaraj, Kumarasamy</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Parasitology international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mishra, Anshuman</au><au>Antony, Justin S</au><au>Gai, Prabhanjan</au><au>Sundaravadivel, Pandarisamy</au><au>Hoang van, Tong</au><au>Jha, Aditya Nath</au><au>Singh, Lalji</au><au>Velavan, Thirumalaisamy P</au><au>Thangaraj, Kumarasamy</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mannose-binding Lectin (MBL) as a susceptible host factor influencing Indian Visceral Leishmaniasis</atitle><jtitle>Parasitology international</jtitle><addtitle>Parasitol Int</addtitle><date>2015-12-01</date><risdate>2015</risdate><volume>64</volume><issue>6</issue><spage>591</spage><epage>596</epage><pages>591-596</pages><issn>1383-5769</issn><eissn>1873-0329</eissn><abstract>Abstract Visceral Leishmaniasis (VL), caused by Leishmania donovani is endemic in the Indian sub-continent. Mannose-binding Lectin (MBL) is a complement lectin protein that binds to the surface of Leishmania promastigotes and results in activation of the complement lectin cascade. We utilized samples of 218 VL patients and 215 healthy controls from an Indian population. MBL2 functional variants were genotyped and the circulating MBL serum levels were measured. MBL serum levels were elevated in patients compared to the healthy controls (adjusted P = 0.007). The MBL 2 promoter variants − 78C/T and + 4P/Q were significantly associated with relative protection to VL (− 78C/T, OR = 0.7, 95% CI = 0.5–0.96, adjusted P = 0.026 and + 4P/Q, OR = 0.66, 95% CI = 0.48–0.9, adjusted P = 0.012). MBL2 * LYQA haplotypes occurred frequently among controls (OR = 0.69, 95% CI = 0.5–0.97, adjusted P = 0.034). MBL recognizes Leishmania and plays a relative role in establishing L. donovani infection and subsequent disease progression. In conclusion, MBL2 functional variants were associated with VL.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>26297290</pmid><doi>10.1016/j.parint.2015.08.003</doi><tpages>6</tpages></addata></record>
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subjects Case-Control Studies
Complement System Proteins - immunology
Cross-Sectional Studies
Female
Gastroenterology and Hepatology
Gene Frequency - genetics
Genotype
Humans
India
Infectious Disease
Leishmania donovani
Leishmania donovani - immunology
Leishmaniasis, Visceral - immunology
Leishmaniasis, Visceral - parasitology
Leishmaniasis, Visceral - pathology
Male
Mannose-Binding Lectin - blood
Mannose-Binding Lectin - genetics
Mannose-Binding Lectin - metabolism
MBL serum level
MBL2
Polymorphism, Single Nucleotide - genetics
Promoter Regions, Genetic - genetics
Visceral Leishmaniasis
title Mannose-binding Lectin (MBL) as a susceptible host factor influencing Indian Visceral Leishmaniasis
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