Role of Mannose-binding Lectin and Association with Microbial Sensitization in a Cohort of Patients with Atopic Dermatitis
Keywords:atopic dermatitis, mannose binding lectin, sensitization immunological, Candida albicans
Atopic dermatitis is a relapsing inflammatory skin condition, in which bacteria, fungi and viruses may colonize the skin and aggravate the condition. Mannose-binding lectin is part of the innate immune system. Polymorphism in the mannose-binding lectin gene can result in deficiency of mannose-binding lectin, which may affect defence against microbes. The aim of this study was to investigate whether polymorphisms in the mannose-binding lectin gene affect the extent of sensitization to common skin microbes, the skin barrier function, or the severity of the disease in a cohort of patients with atopic dermatitis. Genetic testing of mannose-binding lectin polymorphism was performed in 60 patients with atopic dermatitis. The disease severity, skin barrier function, and serum levels of specific immunoglobulin E against skin microbes were measured. In patients with low mannose-binding lectin genotype (group 1) 6 of 8 (75%) were sensitized to Candida albicans, compared to 14 of 22 (63.6%) patients with intermediate mannose-binding genotype (group 2) and 10 of 30 (33.3%) patients with high mannose-binding genotype (group 3). Group 1 (low mannose-binding lectin) was more likely to be sensitized to Candida albicans compared with group 3 (high mannose-binding lectin) (odds ratio 6.34, p-value 0.045). In this cohort of patients with atopic dermatitis, mannose-binding lectin deficiency was associated with increased sensitization to Candida albicans.
Bieber T. Atopic dermatitis. Ann Dermatol 2010; 22: 125-137.
https://doi.org/10.5021/ad.2010.22.2.125 DOI: https://doi.org/10.5021/ad.2010.22.2.125
Leung DY. Infection in atopic dermatitis. Curr Opin Pediatr 2003; 15: 399-404.
https://doi.org/10.1097/00008480-200308000-00008 DOI: https://doi.org/10.1097/00008480-200308000-00008
Sohn MH, Kim CH, Kim WK, Jang GC, Kim KE. Effect of staphylococcal enterotoxin B on specific antibody production in children with atopic dermatitis. Allergy Asthma Proc 2003; 24: 67-71.
Bunikowski R, Mielke M, Skarabis H, Herz U, Bergmann RL, Wahn U, et al. Prevalence and role of serum IgE antibodies to the Staphylococcus aureus-derived superantigens SEA and SEB in children with atopic dermatitis. J Allergy Clin Immunol 1999; 103: 119-124.
https://doi.org/10.1016/S0091-6749(99)70535-X DOI: https://doi.org/10.1016/S0091-6749(99)70535-X
Arzumanyan VG, Magarshak OO, Semenov BF. Yeast fungi in patients with allergic diseases: species variety and sensitivity to antifungal drugs. Bull Exp Biol Med 2000; 129: 601-604.
https://doi.org/10.1007/BF02434889 DOI: https://doi.org/10.1007/BF02434889
Faergemann J. Atopic dermatitis and fungi. Clin Microbiol Rev 2002; 15: 545-563.
https://doi.org/10.1128/CMR.15.4.545-563.2002 DOI: https://doi.org/10.1128/CMR.15.4.545-563.2002
Sonesson A, Bartosik J, Christiansen J, Roscher I, Nilsson F, Schmidtchen A, et al. Sensitization to skin-associated microorganisms in adult patients with atopic dermatitis is of importance for disease severity. Acta Derm Venereol 2013; 93: 340-345.
https://doi.org/10.2340/00015555-1465 DOI: https://doi.org/10.2340/00015555-1465
Back O, Scheynius A, Johansson SG. Ketoconazole in atopic dermatitis: therapeutic response is correlated with decrease in serum IgE. Arch Dermatol Res 1995; 287: 448-451.
https://doi.org/10.1007/BF00373427 DOI: https://doi.org/10.1007/BF00373427
Back O, Bartosik J. Systemic ketoconazole for yeast allergic patients with atopic dermatitis. J Eur Acad Dermatol Venereol 2001; 15: 34-38.
https://doi.org/10.1046/j.1468-3083.2001.00207.x DOI: https://doi.org/10.1046/j.1468-3083.2001.00207.x
Darabi K, Hostetler SG, Bechtel MA, Zirwas M. The role of Malassezia in atopic dermatitis affecting the head and neck of adults. J Am Acad Dermatol 2009; 60: 125-136.
https://doi.org/10.1016/j.jaad.2008.07.058 DOI: https://doi.org/10.1016/j.jaad.2008.07.058
van Asbeck EC, Hoepelman AI, Scharringa J, Herpers BL, Verhoef J. Mannose binding lectin plays a crucial role in innate immunity against yeast by enhanced complement activation and enhanced uptake of polymorphonuclear cells. BMC Microbiol 2008; 8: 229.
https://doi.org/10.1186/1471-2180-8-229 DOI: https://doi.org/10.1186/1471-2180-8-229
Wang M, Chen Y, Zhang Y, Zhang L, Lu X, Chen Z. Mannan-binding lectin directly interacts with Toll-like receptor 4 and suppresses lipopolysaccharide-induced inflammatory cytokine secretion from THP-1 cells. Cell Mol Immunol 2011; 8: 265-275.
https://doi.org/10.1038/cmi.2011.1 DOI: https://doi.org/10.1038/cmi.2011.1
Heitzeneder S, Seidel M, Forster-Waldl E, Heitger A. Mannan-binding lectin deficiency - Good news, bad news, doesn't matter? Clin Immunol 2012; 143: 22-38.
https://doi.org/10.1016/j.clim.2011.11.002 DOI: https://doi.org/10.1016/j.clim.2011.11.002
Madsen HO, Garred P, Thiel S, Kurtzhals JA, Lamm LU, Ryder LP, et al. Interplay between promoter and structural gene variants control basal serum level of mannan-binding protein. J Immunol 1995; 155: 3013-3020.
https://doi.org/10.4049/jimmunol.155.6.3013 DOI: https://doi.org/10.4049/jimmunol.155.6.3013
Carlsson M, Sjoholm AG, Eriksson L, Thiel S, Jensenius JC, Segelmark M, et al. Deficiency of the mannan-binding lectin pathway of complement and poor outcome in cystic fibrosis: bacterial colonization may be decisive for a relationship. Clin Exp Immunol 2005; 139: 306-313.
https://doi.org/10.1111/j.1365-2249.2004.02690.x DOI: https://doi.org/10.1111/j.1365-2249.2004.02690.x
Hammad NM, El Badawy NE, Ghramh HA, Al Kady LM. Mannose-binding lectin: a potential therapeutic candidate against candida infection. Biomed Res Int 2018; 2018: 2813737.
https://doi.org/10.1155/2018/2813737 DOI: https://doi.org/10.1155/2018/2813737
Lillegard JB, Sim RB, Thorkildson P, Gates MA, Kozel TR. Recognition of Candida albicans by mannan-binding lectin in vitro and in vivo. J Infect Dis 2006; 193: 1589-1597.
https://doi.org/10.1086/503804 DOI: https://doi.org/10.1086/503804
Brandao LA, Guimaraes RL, Carrera M, Milanese M, Segat L, Luiz de Lima-Filho J, et al. MBL2 functional allelic variants and increased risk for the development of atopic dermatitis in Brazilian children. Arch Dermatol 2008; 144: 412-413.
https://doi.org/10.1001/archderm.144.3.412 DOI: https://doi.org/10.1001/archderm.144.3.412
Carrera MC, Moura P, Crovella S, de Souza PR, de Alencar LC, Sarinho E. High polymorphism of the MBL2 gene in patients with atopic dermatitis. Ann Allergy Asthma Immunol 2010; 105: 39-42.
https://doi.org/10.1016/j.anai.2010.03.017 DOI: https://doi.org/10.1016/j.anai.2010.03.017
Hashimoto S, Nakamura K, Oyama N, Kaneko F, Fujita T, Tsunemi Y, et al. Mannose-binding lectin (MBL) single nucleotide polymorphism is not associated with atopic dermatitis in Japanese patients. J Dermatol 2005; 32: 1038-1040.
https://doi.org/10.1111/j.1346-8138.2005.tb00897.x DOI: https://doi.org/10.1111/j.1346-8138.2005.tb00897.x
Kim DW, Park JY, Na GY, Lee SJ, Lee WJ. Correlation of clinical features and skin barrier function in adolescent and adult patients with atopic dermatitis. Int J Dermatol 2006; 45: 698-701.
https://doi.org/10.1111/j.1365-4632.2005.02644.x DOI: https://doi.org/10.1111/j.1365-4632.2005.02644.x
Gupta J, Grube E, Ericksen MB, Stevenson MD, Lucky AW, Sheth AP, et al. Intrinsically defective skin barrier function in children with atopic dermatitis correlates with disease severity. J Allergy Clin Immunol 2008; 121: 725-730.e2.
https://doi.org/10.1016/j.jaci.2007.12.1161 DOI: https://doi.org/10.1016/j.jaci.2007.12.1161
Brenninkmeijer EE, Schram ME, Leeflang MM, Bos JD, Spuls PI. Diagnostic criteria for atopic dermatitis: a systematic review. Br J Dermatol 2008; 158: 754-765.
https://doi.org/10.1111/j.1365-2133.2007.08412.x DOI: https://doi.org/10.1111/j.1365-2133.2007.08412.x
Williams HC, Burney PG, Pembroke AC, Hay RJ. The U.K. Working Party's Diagnostic Criteria for Atopic Dermatitis. III. Independent hospital validation. Br J Dermatol 1994; 131: 406-416.
https://doi.org/10.1111/j.1365-2133.1994.tb08532.x DOI: https://doi.org/10.1111/j.1365-2133.1994.tb08532.x
Jönsen A, Bengtsson AA, Sturfelt G, Truedsson L. Analysis of HLA DR, HLA DQ, C4A, FcgammaRIIa, FcgammaRIIIa, MBL, and IL-1Ra allelic variants in Caucasian systemic lupus erythematosus patients suggests an effect of the combined FcgammaRIIa R/R and IL-1Ra 2/2 genotypes on disease susceptibility. Arthritis Res Ther 2004; 6: R557-R562.
https://doi.org/10.1186/ar1224 DOI: https://doi.org/10.1186/ar1224
Jönsen A, Gullstrand B, Guner N, Bengtsson AA, Nived O, Truedsson L, et al. Genetically determined mannan-binding lectin deficiency is of minor importance in determining susceptibility to severe infections and vascular organ damage in systemic lupus erythematosus. Lupus 2007; 16: 245-253.
https://doi.org/10.1177/09612033070160040201 DOI: https://doi.org/10.1177/09612033070160040201
Pinnagoda J, Tupker RA, Agner T, Serup J. Guidelines for transepidermal water loss (TEWL) measurement. A report from the Standardization Group of the European Society of Contact Dermatitis. Contact Dermatitis 1990; 22: 164-178.
https://doi.org/10.1111/j.1600-0536.1990.tb01553.x DOI: https://doi.org/10.1111/j.1600-0536.1990.tb01553.x
Schmitt J, Langan S, Williams HC, European Dermato-Epidemiology N. What are the best outcome measurements for atopic eczema? A systematic review. J Allergy Clin Immunol 2007; 120: 1389-1398.
https://doi.org/10.1016/j.jaci.2007.08.011 DOI: https://doi.org/10.1016/j.jaci.2007.08.011
Severity scoring of atopic dermatitis: the SCORAD index. Consensus Report of the European Task Force on Atopic Dermatitis. Dermatology 1993; 186: 23-31.
https://doi.org/10.1159/000247298 DOI: https://doi.org/10.1159/000247298
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Copyright (c) 2023 Emma Belfrage, Camilla L. Jinnestål, Andreas Jönsen, Anders Bengtsson, Anna Åkesson, Artur Schmidtchen, Andreas Sonesson
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