РОЛЬ ГЕНЕТИЧНИХ МОДИФІКАЦІЙ ФАКТОРІВ ПРИРОДНОГО ІМУНІТЕТУ ПРИ МЕНІНГІТІ

V. I. Shulyak

Анотація


Менінгіт (М) є небезпечним для життя інфекційним захворюванням центральної нервової системи, проблема лікування якого залишається актуальною у зв’язку з великим відсотком ускладнень і залишкових явищ. Серед систем організму, що забезпечують успіх боротьби з інфекцією, провідну роль відіграє імунітет, який включає фактори природної (вродженої) і адаптивної (набутої) ланки. Фактори природного імунітету забезпечують захист організму на початковому етапі від більшості збудників, здатних викликати М. Дефекти генів, відповідальних за фактори природного імунітету, створюють умови, коли організм не може впоратися з патогенами, внаслідок чого макроорганізм вибудовує міцнішу оборону за допомогою адаптивного імунітету.


Ключові слова


менінгіт; природний імунітет; гени; однонуклеотидний поліморфізм.

Повний текст:

тут

Посилання


Heckenberg, S. G., de Gans, J., Brouwer, M. C. (2008). Clinical features, outcome, and meningococcal genotype in 258 adults with meningococcal meningitis: a prospective cohort study. Medicine (Baltimore), 87(4), 185-192.

Brouwer, M. C., Tunkel, A. R., van de Beek, D. (2010). Epidemiology, diagnosis, and antimicrobial treatment of acute bacterial meningitis. Clin. Microbiol. Rev., 23, 467-492.

Nikiforov, V. A., Kichikova, V. V., Yefimov, Ye. I. (2011). Aktual'nyye i nereshennyye problemy meningokokkovoy infektsii na sovremennom etape. Meditsinskiy al'manakh, (4), 94-99.

Zabbarova, A. T. (2013). Gidrotsefaliya posle perenesennogo meningita: sovremennoye sostoyaniye problemy. Vestnik sovremennoy klinicheskoy meditsiny (Kazan'), 6(3), 99-100.

Skripchenko, N. V., Kulikova, K. A. (2014). Sovremennyye patofiziologicheskiye aspekty bakterial'nykh meningoentsefalitov. Infektsionnyye bolezni, 12(2), 76-82.

Steens, A., Eriksen, H.-M., Blystad, H. (2014). What are the most important infectious diseases among those ≥65 years: a comprehensive analysis on notifiable diseases, Norway, 1993–2011. BMC Infectious Diseases, (14), 57.

Hart, J. Jr., Tillman, G., Kraut, M. A. (2014). NIAID Collaborative Antiviral Study Group West Nile Virus 210 Protocol Team. West Nile virus neuroinvasive disease: neurological manifestations and prospective longitudinal outcomes. BMC Infect. Dis., (14), 248.

Heckenberg, S. G., Brouwer, M. C., van de Beek, D. (2014). Bacterial meningitis. Handb. Clin. Neurol., 121, 1361-1375.

Skoczyсska, A., Kadіubowski, M., Knap, J. (2006). Invasive meningococcal disease associated with a very high case fatality rate in the North-West of Poland. FEMS Immunol. Med. Microbiol., 46(2), 230-235.

Harboe, Z. B., Thomsen, R. W., Riis, A. (2009). Pneumococcal serotypes and mortality following invasive pneumococcal disease: a population-based cohort study. PLoS Med., 6(5), e:1000081.

Rubach, M. P., Bender, J. M., Mottice, S. (2011). Increasing incidence of invasive Haemophilus influenzae disease in adults, Utah, USA. Emerg. Infect. Dis., 17(9), 1645-1650.

McIntyre, P. B., O'Brien, K. L., Greenwood, B., van de Beek, D. (2012). Effect of vaccines on bacterial meningitis worldwide. Lancet, 380(9854), 1703-1711.

Vengerov YU. YA. (2013). Pnevmokokkovyy meningit. Problema vysokoy letal'nosti. Lechashchiy vrach, (5), 14-16.

Ladhani S. N. (2013). Invasive pneumococcal disease after routine pneumococcal conjugate vaccination in children, England and Wales. Emerg. Infect. Dis., 19(1), 61-68.

Imцhl, M., Mцller, J., Reinert, R. (2015). Pneumococcal meningitis and vaccine effects in the era of conjugate vaccination: results of 20 years of nationwide surveillance in Germany. BMC Infectious Diseases, (15), 61.

Crawford, D. C., Zimmer, S. M., Morin, C. A. (2008). Integrating host genomics with surveillance for invasive bacterial diseases. Emerg. Infect. Dis., 14(7), 1138-1140.

Hjuler, T., Poulsen, G., Wohlfahrt, J. (2008). Genetic susceptibility to severe infection in families with invasive pneumococcal disease. Am. J. Epidemiol., 167(7), 814-819.

Brouwer, M. C., de Gans, J., Heckenberg S. G. (2009). Host genetic susceptibility to pneumococcal and meningococcal disease: a systematic review and meta-analysis. Lancet Infect. Dis., 9(1), 31-44.

Lyons, E. J., Amos, W., Berkley, J. A. (2009). Homozygosity and risk of childhood death due to invasive bacterial disease. BMC Med. Genet., (10), 55.

Brouwer, M. C., Read, R. C., van de Beek, D. (2010). Host genetics and outcome in meningococcal disease: a systematic review and meta-analysis. Lancet Infect. Dis., (10), 262-274.

Loeb, M., Eskandarian, S., Rupp, M. (2011). Genetic variants and susceptibility to neurological complications following West Nile virus infection. J. Infect. Dis., 204(7), 1031-1037.

Sanders, M. S., van Well, G. T., Ouburg, S., Morrй, S. A., van Furth, A. M. (2011). Genetic variation of innate immune response genes in invasive pneumococcal and meningococcal disease applied to the pathogenesis of meningitis. Genes Immun., 12(5), 321-334.

Cruc, M., Franзois, N., Gentile, A. (2013). Why meningococcal meningitis is still lethal: response in genes? Presse Med., 42(3), 363-365.

Lavezzo, E., Toppo, S., Franchin, E. (2013). Genomic comparative analysis and gene function prediction in infectious diseases: application to the investigation of a meningitis outbreak. BMC Infectious Diseases, (13), 554.

Sanders, M. S., de Jonge, R. C., Terwee, C. B. (2013). Addition of host genetic variants in a prediction rule for post meningitis hearing loss in childhood: a model updating study. BMC Infect. Dis., 23(13), 340.

Ginter, Ye. K. (2003). Meditsinskaya genetika. M.: Meditsina.

Bochkov N. P. (2002). Klinicheskaya genetika: uchebnik. M.: GEOTAR – MED.

Yarilin A. A. (2010). Immunologiya. M.: GEOTAR-Media.

Abdelmalek, R., Kallel Sallemi, M., Zerzri, Y. (2011). Hereditary complement deficiency in Tunisian adults with purulent meningitis. Med. Mal. Infect., 41(4), 206-208.

Skattum L., van Deuren, M., van der Poll, T., Truedsson, L. (2011). Complement deficiency states and associated infections. Mol. Immunol., 48(14), 1643-1655.

Adriani, K. S., Brouwer, M. C., Geldhoff, M. (2013). Common polymorphisms in the complement system and susceptiblity to bacterial meningitis. J. Infect., 66(3), 255-262.

Jaatinen, T., Lahti, M., Ruuskanen, O. (2003). Total C4B deficiency due to gene deletion and gene conversion in a patient with severe infections. Clin. Diagn. Lab. Immunol., 10 (2), 195-201.

Vardar, F., Pehlivan, S., Onay, H. (2007). Association between mannose binding lectin polymorphisms and predisposition to bacterial meningitis. Turk. J. Pediatr., 49(3), 270-273.

Lima Filho, A., Carmo, R., Cavalcanti, M. (2012). Complement and mannose-binding lectin 2 polymorphism in meningococcal disease. Clin. Lab., 58(11-12), 1165-1169.

Brouwer, M. C., Baas, F., van der Ende, A., van de Beek, D. (2013). Genetic variation and cerebrospinal fluid levels of mannose binding lectin in pneumococcal meningitis patients. PLoS One, 8(5), e:65151.

Jaatinen, T., Lahti, M., Ruuskanen, O. (2003). Total C4B deficiency due to gene deletion and gene conversion in a patient with severe infections. Clin. Diagn. Lab. Immunol., 10(2), 195-201.

Lundbo, L. F., Harboe, Z. B., Clausen, L. N. (2014). Mannose-binding lectin gene, MBL2, polymorphisms are not associated with susceptibility to invasive pneumococcal disease in children. Clin. Infect. Dis., 59(4), 66-71.

Fries, L. F., O'Shea, J. J., Frank, M. M. (1986). Inherited deficiencies of complement and complement-related proteins. Clin. Immuno. Immunopathol., 40(1), 37-49.

Woehrl, B., Brouwer, M. C., Murr, C. (2011). Complement component 5 contributes to poor disease outcome in humans and mice with pneumococcal meningitis. J. Clin. Invest., 121(10), 3943-3953.

Orren, A., Owen, E. P., Henderson, H. E. et al. (2012). Complete deficiency of the sixth complement component (C6Q0), susceptibility to Neisseria meningitidis infections and analysis of the frequencies of C6Q0 gene defects in South Africans. Clin. Exp. Immunol., 167(3), 459-471.

Schirinzi, R., Lantin, J. P., Frйmeaux-Bacchi, V., Schifferli, J. A., Trendelenburg M. (2006). Combined-heterozygous deficiency of complement C7 in a patient with recurrent meningitis. Med. Klin. (Munich), 101(8), 655-658.

Arnold, D. F., Roberts, A. G., Thomas, A. (2009). A novel mutation in a patient with a deficiency of the eighth component of complement associated with recurrent meningococcal meningitis. Clin. Immunol., 29(5), 691-695.

Seitsonen, S., Helminen, M., Jarva, H., Meri, S., Jдrvelд, I. (2010). Properdin mutations a risk factor for meningitis. Duodecim, 126(9), 1071-1075.

Bathum, L., Hansen, H., Teisner, B. (2006). Association between combined properdin and mannose-binding lectin deficiency and infection with Neisseria meningitidis. Mol. Immunol., 43(5), 473-479.

Bodiyenkova, G. M., Titova, ZH. V. (2015). Rol' polimorfizma i ekspressii otdel'nykh genov tsitokinov v formirovanii patologii (Obzor). Uspekhi sovremennogo yestestvoznaniya, (1-4), 616-620.

Konenkov, V. I., Smol'nikova, M. V. (2003). Strukturnyye osnovy i funktsional'naya znachimost' allel'nogo polimorfizma genov tsitokinov cheloveka i ikh retseptorov. Meditsinskaya immunologiya, 5(1-2), 11-28.

Carrol, E. D., Payton, A., Payne, D. (2011). The IL1RN promoter rs4251961 correlates with IL-1 receptor antagonist concentrations in human infection and is differentially regulated by GATA-1. J. Immunol., 186(4), 2329-2335.

Titmarsh, C. J., Moscovis, S. M., Hall, S. (2013). Comparison of cytokine gene polymorphisms among Greek patients with invasive meningococcal disease or viral meningitis. J. Med. Microbiol., 62(5), 694-700.

Oztuzcu, S., Cakmak, E. A., Sivasli, E. (2011). Gene expression and promoter region polymorphisms of interleukin-10 in meningitis patients. Genet. Test. Mol. Biomarkers, 15(5), 327-331.

Abaturov, A. Ye. (2007). Rol' interferonov v zashchite respiratornogo trakta. Chast' 1. Kaskad vozbuzhdeniya sistemy interferonov. Zdorov'ye rebenka, (5), 8.

Mьller, U., Steinhoff, U., Reis, L.F. et al. (1994). Functional role of type I and type II interferons in antiviral defense. Science, 264(5167), 1918-1921.

Dale, D. C., Boxer, L., Liles, W. C. (2008). The phagocytes: neutrophils and monocytes. Blood, 112(4), 935-945.

Lange, C., Dьrr, C. M., Doster, H. (2007). Dendritic cell-regulatory T-cell interactions control self-directed immunity. Immunol. Cell. Biol., 85(8), 575-581.

Vorob'yeva, N. V. (2015). Molekulyarnyye mekhanizmy fagotsitoza. Obzor. Chast' 2. Rossiyskiy immunologicheskiy zhurnal, 9(18), 1, 5-13.

Kumagai, Y., Takeuchi, O., Akira, S. (2008). Pathogen recognition by innate receptors. J. Infect. Chemother., 14(2), 86-92.

Randhawa, A. K., Hawn, T. R. (2008). Toll-like receptors: their roles in bacterial recognition and respiratory infections. Expert. Rev. Anti. Infect. Ther., 6(4), 479-495.

Koval'chuk, L. V., Svitich, O. A., Gankovskaya, L. V., Mironshichenkova, A. M., Gankovskiy, V. A. (2012). Rol' Toll-podobnykh retseptorov v patogeneze infektsionnykh zabolevaniy cheloveka. Kurskiy nauchno-prakticheskiy vestnik «Chelovek i yego zdorov'ye», (2), 56-60.

Abaturov, A. Ye., Volosovets, A. P., Yulish, Ye. I. (2012). Rol' Toll-podobnykh retseptorov v rekognitsii patogen-assotsiirovannykh molekulyarnykh struktur infektsionnykh patogennykh agentov i razvitii vospaleniya. Chast' 1. Semeystvo TLR. Zdorov'ye rebenka, (1), 154-159.

Abaturov, A. Ye., Volosovets, A. P., Yulish, Ye. I. (2012). Rol' Toll-podobnykh retseptorov v rekognitsii patogen-assotsiirovannykh molekulyarnykh struktur infektsionnykh patogennykh agentov i razvitii vospaleniya. Chast' 3. Rekognitsiya ligandov TLR. Zdorov'ye rebenka, (7), 157-164.

Sanders, M. S., van Well, G. T., Ouburg, S. (2011). Single nucleotide polymorphisms in TLR9 are highly associated with susceptibility to bacterial meningitis in children. Clin. Infect. Dis., 52(4), 475-480.

Sanders, M. S., van Well, G. T., Ouburg, S., Morrй, S. A., van Furth, A. M. (2012). Toll-like receptor 9 polymorphisms are associated with severity variables in a cohort of meningococcal meningitis survivors. BMC Infect. Dis., (12), 112.

van Well, G. T., Sanders, M. S., Ouburg, S., van Furth, A. M., Morrй S. A. (2012). Polymorphisms in Toll-like receptors 2, 4, and 9 are highly associated with hearing loss in survivors of bacterial meningitis. PLoS One, 7(5), e35837.

van Well, G. T., Sanders, M. S., Ouburg, S. (2013). Single nucleotide polymorphisms in pathogen recognition receptor genes are associated with susceptibility to meningococcal meningitis in a pediatric cohort. PLoS One, 8(5), e64252.

Barkhash, A. V., Voevoda, M. I., Romaschenko, A. G. (2013). Association of single nucleotide polymorphism rs3775291 in the coding region of the TLR3 gene with predisposition to tick-borne encephalitis in a Russian population. Antiviral. Res., 99(2), 136-138.

Ting, J. P., Lovering, R. C., Alnemri, E. S. (2008). The NLR gene family: a standard nomenclature. Immunity, 28(3), 285-287.

Abaturov, A. Ye., Volosovets, A. P., Yulish, Ye. I. (2013). Rol' NOD-podobnykh retseptorov v rekognitsii patogen-assotsiirovannykh molekulyarnykh struktur infektsionnykh patogennykh agentov i razvitii vospaleniya. Chast' 3a. Proteiny NLR semeystva, uchastvuyushchiye v aktivatsii ASC-assotsiirovannogo puti vozbuzhdeniya.. Inflammasomy. Zdorov'ye rebenka, (3), 140-147.

Martinon, F., Mayor, A., Tschopp, J. (2009). The inflammasomes: guardians of the body. Annu. Rev. Immunol., (27), 229-265.

Geldhoff, M., Mook-Kanamori, B. B., Brouwer, M. C. (2013). Genetic variation in inflammasome genes is associated with outcome in bacterial meningitis. Immunogenetics, 65(1), 9-16.

Witzenrath, M., Pache, F., Lorenz, D. (2011). The NLRP3 inflammasome is differentially activated by pneumolysin variants and contributes to host defense in pneumococcal pneumonia. J. Immunol., 187(1), 434-440.

Costa, A., Gupta, R., Signorino, G. (2012). Activation of the NLRP3 inflammasome by group B streptococci. J. Immunol., 188(4), 1953-1960.

Satoh, T., Kato, H., Kumagai, Y. (2010). LGP2 is a positive regulator of RIG-I- and MDA5-mediated antiviral responses. Proc. Nat.. Acad. Sci. USA, 107(4), 1512-1517.

Abaturov, A. Ye., Volosovets, A. P., Yulish, Ye. I. (2013). Rol' RIG-podobnykh retseptorov v rekognitsii patogen-assotsiirovannykh molekulyarnykh struktur infektsionnykh patogennykh agentov i razvitii vospaleniya. Chast' 1. Semeystvo RLR. Zdorov'ye rebenka, (6), 177-183.

Komuro, A., Horvath, C. M. (2007). RNA- and virus-independent inhibition of antiviral signaling by RNA helicase LGP2. J. Virol., 80(24), 12332–12342.

Lakhtin, V. M., Lakhtin, M. V., Afanas'yev, S. S. (2008). Obshchiye svoystva i printsipy funktsionirovaniya lektinov v biosistemakh. Vestnik RAMN, (3), 37-42.

Mittal, R., Sukumaran, S. K., Selvaraj, S. K. (2010). Fcг receptor I alpha chain (CD64) expression in macrophages is critical for the onset of meningitis by Escherichia coli K1. PLoS Pathog., 6(11), e1001203.

Tezcan, I., Berkel, A.I., Ersoy, F., Sanal, O., Kanra, G. (1998). Fc gamma receptor allotypes in children with bacterial meningitis. A preliminary study. Turk. J. Pediatr., 40(4), 533-538.

Bouglй, A., Max, A., Mongardon, N. et al. (2012). Protective effects of FCGR2A polymorphism in invasive pneumococcal diseases. Chest, 142(6), 1474-1481.

Fang, F. C. (2004). Antimicrobial reactive oxygen and nitrogen species: concepts and controversies. Nat. Rev. Microbiol., 2(10), 820-832.

Shatwell, K. P., Segal, A. W. (1996). NADPH oxidase. Int. J. Biochem. Cell Biol., 28(11), 1191-1195.

Klebanoff, S. J. (1999). Myeloperoxidase. Proc. Assoc. Am. Physicians, 111(5), 383-389.

Mills, E. L., Quie, P. G. (1980). Congenital disorders of the function of polymorphonuclear neutrophils. Rev. Infect. Dis., 2(3), 505-517.

Payton, A., Payne, D., Mankhambo, L.A. (2009). Nitric oxide synthase 2A (NOS2A) polymorphisms are not associated with invasive pneumococcal disease. BMC Med. Genet., 23(10), 28.

Brandenburg, L.O., Varoga, D., Nicolaeva, N. (2008). Role of glial cells in the functional expression of LL-37 rat cathelin-related antimicrobial peptide in meningitis. J. Neuropathol. Exp. Neurol., 67(11), 1041-1054.

Ricevuti, G. (1997). Host tissue damage by phagocytes. Ann. N. Y. Acad. Sci., (832), 426-448.

Barkhash, A.V., Perelygin, A.A., Babenko, V.N. (2012). Single nucleotide polymorphism in the promoter region of the CD209 gene is associated with human predisposition to severe forms of tick-borne encephalitis. Antiviral. Res., 93(1), 64-68.




DOI: http://dx.doi.org/10.11603/1681-2727.2016.4.7221

Посилання

  • Поки немає зовнішніх посилань.