Advertisement

The Effect of Respiratory Virus Infection on Expression of Cell Surface Antigens Associated with Binding of Potentially Pathogenic Bacteria

  • O. R. Elahmer
  • M. W. Raza
  • M. M. Ogilvie
  • C. C. Blackwell
  • D. M. Weir
  • R. A. Elton
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 408)

Abstract

Serious secondary bacterial infection can occur following illness due to respiratory viruses and viral infections have also been suggested to be predisposing factors for bacterial meningitis [Moore et al., 1990; Cartwright et al., 1991]. Respiratory virus infection can compromise host defences against bacterial infection in a number of ways: immune suppression; diminished phagocytosis by polymorphonuclear leucocytes; local tissue injury; loss of mucociliary function and decreased bacterial clearance; formation of exudates that enhance bacterial growth; and increased bacterial binding to virus infected cells. Most investigators have studied associations of influenza virus and respiratory pathogens such as Streptococcus pneumoniae [Plotkowski et al., 1986], Staphylococcus aureus [Musher and Fainstein, 1981] and Haemophilus influenzae [Bakeletz et al., 1988; Fainstein et al.,1980].

Keywords

Respiratory Syncytial Virus Bacterial Meningitis Invasive Pneumococcal Disease Neisseria Meningitidis Bordetella Pertussis 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. Alkout AH, Blackwell CC, Weir DM, Luman W, Palmer K. Adhesin of Helicobacter pylori that binds to H type 2 and Lewis blood groups: an explanation of increased susceptibility of blood group O and non-secretors to peptic ulcers. In Toward Anti-Adhesin Therapy of Microbial Diseases Ed. I. Kahane and I. Ofek PlenumGoogle Scholar
  2. Cartwright KAV, Jones DM, Smith AJ, Stuart JM, Kaczmarski EB, Palmer SR. Influenza A and meningococcal disease. Lancet 1991; 338: 554–557.CrossRefGoogle Scholar
  3. Ejlertsen T, Thisted E, Ebbesen F, Olesen B, Renneberg J. Branhamella catarrhalis in children and adults. A study of prevalence, time of colonisation, and association with upper and lower respiratory tract infections. J Infect 1994; 29: 23–31.PubMedCrossRefGoogle Scholar
  4. Falsey AR, Cunningham CK, Barker WH, Kovides RW. Respiratory syncytial virus and influenza A infection in hospitalized elderly. J Infect Dis 1995; 172: 389–394.PubMedCrossRefGoogle Scholar
  5. Gutmann L, Williamson R, Moreau N, Kitzis M-D, Collatz E, Acar JF, Goldstein FW. Cross resistance to naladixic acid, trimethoprim and chloramphenicol associated with alterations in outer-membrane proteins of Klebsiella, Enterobacter and Serratia. J Infect Dis 1985; 151: 501–507.PubMedCrossRefGoogle Scholar
  6. Hancock IC, Poxton IR. Bacterial cell surface techniques. John Wiley and Sons Ltd. Chichester: 1988.Google Scholar
  7. Helminen ME, Mclver I, Latimer JL, Cope LD, McCracken GH, Hansen EJ. A major outer membrane protein of Moraxella catarrhalis is a target for antibodies that enhance pulmonary clearance of the pathogen in an animal model. Infect Immun 1993; 61: 2003–2100.PubMedGoogle Scholar
  8. Helminen ME, McIver I, Paris J, Latimer JL, Lumbley SL, Cope LD, McCracken GH, Hansen EJ. A mutation affecting expression of a major outer membrane protein of Moraxella catarrhalis alters serum resistance and survival in vivo. J Infect Dis 1993; 168: 1194–1201.PubMedCrossRefGoogle Scholar
  9. Kim PE, Musher DM, Glezen WP, Rodriguez-Barradas MC, Nahm WK, Wright CE. Association of invasive pneumococcal disease with season, atmospheric conditions, air pollution and the isolation of respiratory viruses. Clin Infect Dis 1996; 22: 100–106.PubMedCrossRefGoogle Scholar
  10. Korppi M, Matila ML, Jaaskelainen J, Leinonen M. Role of Moraxella (Branhamella) catarrhalis as a respiratory pathogen in children. Acta Pediatrica 1992; 81: 993–996.CrossRefGoogle Scholar
  11. Korppi M, Leinonen M, Koskala M, Makela H, Launiala K. Bacterial coinfection in children hospitalised with respiratory syncytial virus. Pediatr Infect Dis 1989; 8: 687–692.CrossRefGoogle Scholar
  12. Moore PS, Hierholzer J, De Witt W, Gount K, Lippveld T, Plikaytis B, Broome CV. Respiratory viruses and mycoplasma as cofactors for epidemic group A meningococcus meningitis J Am Med Assoc 1990; 264: 1271–1275.CrossRefGoogle Scholar
  13. Nelson WJ, Hopkins RS, Roe MH, Glode MP. Simultaneous infection with Bordetella pertussis and respiratory syncytial virus in hospitalized children. Pediatr Infect Dis 1986; 5: 540–544.PubMedCrossRefGoogle Scholar
  14. Pressman BC. Biological application of ionophores. Ann Rev Biochem 1976; 45: 501–530.PubMedCrossRefGoogle Scholar
  15. Raza MW. Viral infections as predisposing factors for bacterial meningitis. PhD Thesis University of Edinburgh 1992.Google Scholar
  16. Raza MW, Ogilvie MM, Blackwell CC, Stewart J, Elton RA, Weir DM. Effect of respiratory syncytial virus infection on binding of Neisseria meningitidis and type b Haemophilus influenzae to human epithelial cell line (HEp-2). Epidemiol Infect 1993; 110: 339–347.PubMedCrossRefGoogle Scholar
  17. Raza MW, Blackwell C., Ogilvie MM, Saadi AT, Stewart J, Elton RA, Weir DM. Evidence for the role of glycoprotein G of respiratory syncytial virus in binding to Neisseria meningitidis to HEp-2 cells. FEMS Immunol Med Microbiol. 1994; 10: 25–30.PubMedCrossRefGoogle Scholar
  18. Ruuskanen O, Ogra PL. Respiratory syncytial virus Curr Prob Pediat 1993; 23: 50–79.CrossRefGoogle Scholar
  19. Saadi AT, Blackwell CC, Mackenzie DAC, Busuttil A, Raza MW, Essery SD, Weir DM, Elton RA, Brooke H, Gibson AAM. Immunisation against Bordetella pertussis and the decline in SIDS in southeast Scotland. Third SIDS International Congress. 1994; p. 118.Google Scholar
  20. Saadi AT, Blackwell CC, Raza MW, James VS, Stewart J, Elton RA, Weir DM. Factors enhancing adherence of toxigenic Staphylococcus aureus to epithelial cells and their possible role in sudden infant death syndrome. Epidemiol Infect 1993; 110: 507–517.PubMedCrossRefGoogle Scholar
  21. Saadi AT, Weir DM, Poxton IR, Stewart J, Essery SD, Raza MW, Blackwell CC, Busuttil A. Isolation of an adhesin from Staphylococcus aureus that binds Lewisa blood group antigen and its relevance to sudden infant death syndrome. FEMS Immunol Med Microbiol 1994; 8: 315–320.PubMedCrossRefGoogle Scholar
  22. Saadi AT, Blackwell CC, Essery SD, Raza MW, Weir DM, Elton RA, Busuttil, A, Keeling JW. Developmental and environmental factors that enhance binding of Bordetella pertussis to human epithelial cells in relation to sudden infant death syndrome. (submitted for publication)Google Scholar
  23. Schlesinger LS, Horwitz MA. Phagocytosis of Mycobacterium leprae by human monocyte derived macrophages is mediated by complement receptors CR1 (CD35), CR3 (CDllb/CD18) and CR4(CD 11 c/CD 18) and INFγ activation inhibits complement receptor function and phagocytosis of this bacterium. J Immunol 1991; 147: 1983–1994.PubMedGoogle Scholar
  24. van t’Wout J, Burnette WN, Mar VL, Rozdzinski E, Wright SD, Tuomanen E. Role of carbohydrate recognition domains of pertussis toxin in adherence of Bordetella pertussis to human macrophages. Infect Immun 1992; 60: 3303–3308.Google Scholar
  25. Wright SD, Jong MTC. Adhesion-promoting receptors on human macrophages recognize Escherichia coli by binding to lipopolysaccharide. J Exp Med 1986; 164: 1876–1888.PubMedCrossRefGoogle Scholar
  26. Ziegler-Heitbrock WL, Ulevitch RJ. CD 14 cell surface receptor and differentiation marker. Immunol Today 1993; 14:121–125.CrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1996

Authors and Affiliations

  • O. R. Elahmer
    • 1
  • M. W. Raza
    • 1
  • M. M. Ogilvie
    • 1
  • C. C. Blackwell
    • 1
  • D. M. Weir
    • 1
  • R. A. Elton
    • 1
  1. 1.Department of Medical MicrobiologyUniversity of EdinburghEdinburghScotland

Personalised recommendations