Contribution of Lewis blood groups molecules in biofilm formation of Pseudomonas aeruginosa isolated from atopic dermatitis patients.


  • Fatima Rammadan Abdul Department of Biology, College of Science, Mustansiriyah University
  • Khedhir H. Ali Department of Biology, College of Science, Mustansiriyah University



Key Words, - Lewis blood groups – Pseudomonas aeruginosa -atopic dermatitis– Biofilm


Abstract Biofilm formation is a mechanism for bacterial community defense against insults including antibiotics .In this report we evaluated the potency of Pseudomonas aeruginosa(P. aeruginosa) isolates from atopic dermatitis patients skin as well as stool to colonize different Lewis types saliva , manifested by biofilm formation . The bacteria were cultured on tryptose soy broth .96-well polystyrene plate were used .Coating with heat inactivated Le (a), (b) and (c)saliva was performed. Biofilm intensity was measured using crystal violet stained films compared to non –saliva coated situation. The results showed a superior capability of most isolates to form biofilm on Le (a) followed by Le (b) saliva. The highest binding mean was for isolate ( 4). Le (a) saliva binding (mean ± SD was 0.66± 0.25 for test compared to 0.21± 0.04 for control non coated wells) , p=0.04,cl=0.041-0.864. Other isolates demonstrated variable degree of biofilm formation on this substrate .In contrast to Le (c) saliva, Le (b) saliva demonstrated weak biofilm formation . We conclude that, among atopic dermatitis patients skins, P. aeruginosa Lec (A) or Lec (B) lectins might be involved in colonization in such patients. Key Words:- Lewis blood groups – Pseudomonas aeruginosa -atopic dermatitis– Biofilm


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Author Biography

  • Fatima Rammadan Abdul, Department of Biology, College of Science, Mustansiriyah University



Ahmed T,Lundgren A,Arifuzzaman M,Qadri F.Teneberg S.Svennerholm A M. 2009.Children with the Le(a+b-) blood groups have increased susceptibility to diarrhea caused by enterotoxicogenic , Escherichia coli expressing colonization factor1 group fimbriae .Inf.Immun.77:2059-2064.

Subhi HT. 2015.Inhibition of biofilm formation of Pseudomonas aeruginosa isolated from colorectal cancer and ulcerative colitis using iron oxide nanoparticle composites. Ph.D. thesis, university of Al-Mustansiryiah. College of Science.

Kipnis E, Sawa T, Wiener-Krmish .2000.Targating mechanisms of Pseudomonas aeruginosa pathogenesis .Med.Mal.Infect.36:78-91.

Bjarnsho H T.2013.The role of bacterial biofilm in chronic infections. APMIS.121:1-58.

Grishin AV, Krivozubou MS,Karyagina AS,Gintsburg AL.2015. Pseudomonas aeruginosa lectins as targets for novel antibacterials .Acta Nature.7:29-41.

Cioci G, Mitchell EP,Gaatier C,Wimmerova M, Sudakevitz D,Perez S, Gilboa-Garber N,Imberty A.2003.Structural basis of Calcium and galactose recognition by the lectin PA-1L of Pseudomonas aeruginosa .FEBS let.4:297-301.

Mitchell E, Houles C, Sudakevitz D, Wimmerova M, Gautier C, Pérez S, Wu A.M, Gilboa-Garber N, Imberty A. 2002. Structural basis for oligosaccharide-mediated adhesion of Pseudomonas aeruginosa in the lungs of cystic fibrosis patients, Nature Struct. Biol., 9: 918–921.

Thomsson K.A, Schulz B.L, Packer NH, KarlssonN G. 2005. MUC5B glycosylation in human saliva reflects blood group and secretor status, Glycobiology, 15:791-804.

Agarwal A, Singh K P, Jain A.2010.Medical significance and management of Staphlylococcal biofilm .FEMS. Immunol .Med .Microbiol.58:147-160.

Baker BS.2006.The role of microorganisms in atopic dermatitis .Clin.Exp.Immunol.144:1-9.

Derrien M,VenPassel M W J, Van de Boven Kamp J H B ,Schipper R G, deVos W M ,Dekker J. 2010.Mucin – bacterial interactions in the human oral cavity and digestive tract.Gut.Microbes.1:254-268.

Sommer R, Hauck D,Varrot A,Wagner S,Audfray A, Prestel A, Molker HM,Imberty A,Titz A.2015. Cinnamide derivatives of d-Mannose as inhibitors of the bacterial virulence factor lec B from Pseudomonas aeruginosa .Chemistry.Ooen.4:756-67.

Johansson E M ,Crusz SA, Kolomiet E, Buts L ,Kadam R U,Cacciarini M,Bartels K M ,Diggle S P,Camara M,Williams P, Loris R, Nativi c, Rosenau F,Jaeger K E, Dorbre T, Reymond J L,.2008.Ihibition and dispersion of Pseudomonas aeruginosa biofilms by glycopeptide dendrimers targating the fucose-specific lectin Lec B.Chem.Biol.15:1249-57.

Tielker D,Hacker S, Loris R, Strathmann M,Wingender J,Wilhelm S,Rosenau F, Jaeger KE. Pseudomonas aeruginosa lectin B IS located in the outer membrane and is involved in biofilm formation. Microbiology .151:1313-23.

Biesbrock A R,Reddy MS,Levine M J.1991.Interaction of a salivary mucin – secretory Immunoglobulin A complex with mucosal pathogens.Infect.Immunil.59:3492-3497.


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Original Article

How to Cite

F. R. Abdul and K. H. Ali, “Contribution of Lewis blood groups molecules in biofilm formation of Pseudomonas aeruginosa isolated from atopic dermatitis patients”., Al-Mustansiriyah Journal of Science, vol. 29, no. 2, pp. 69–73, Nov. 2018, doi: 10.23851/mjs.v29i2.302.

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