title: Cefditoren and ceftriaxone enhance complement-mediated immunity in the presence of specific antibodies against antibiotic-resistant pneumococcal strains.
abstract: BACKGROUND
  Specific antibodies mediate humoral and cellular protection against invading pathogens such as Streptococcus pneumoniae by activating complement mediated immunity, promoting phagocytosis and stimulating bacterial clearance. The emergence of pneumococcal strains with high levels of antibiotic resistance is of great concern worldwide and a serious threat for public health.
  
  
  RESULTS
  Flow cytometry was used to determine whether complement-mediated immunity against three antibiotic-resistant S. pneumoniae clinical isolates is enhanced in the presence of sub-inhibitory concentrations of cefditoren and ceftriaxone. The binding of acute phase proteins such as C-reactive protein and serum amyloid P component, and of complement component C1q, to pneumococci was enhanced in the presence of serum plus either of these antibiotics. Both antibiotics therefore trigger the activation of the classical complement pathway against S. pneumoniae. C3b deposition was also increased in the presence of specific anti-pneumococcal antibodies and sub-inhibitory concentrations of cefditoren and ceftriaxone confirming that the presence of these antibiotics enhances complement-mediated immunity to S. pneumoniae.
  
  
  CONCLUSIONS
  Using cefditoren and ceftriaxone to promote the binding of acute phase proteins and C1q to pneumococci, and to increase C3b deposition, when anti-pneumococcal antibodies are present, might help reduce the impact of antibiotic resistance in S. pneumoniae infections.
authors.affiliation: Centro de Investigaciones Biológicas, and CIBER de Enfermedades Respiratorias, Madrid, Spain.
authors.forename: Elisa
authors.initials: E
authors.lastname: Ramos-Sevillano
authors.forename: Cinthya
authors.initials: C
authors.lastname: Rodríguez-Sosa
authors.forename: Fabio
authors.initials: F
authors.lastname: Cafini
authors.forename: Maria-Jose
authors.initials: MJ
authors.lastname: Giménez
authors.forename: Ana
authors.initials: A
authors.lastname: Navarro
authors.forename: David
authors.initials: D
authors.lastname: Sevillano
authors.forename: Luis
authors.initials: L
authors.lastname: Alou
authors.forename: Ernesto
authors.initials: E
authors.lastname: García
authors.forename: Lorenzo
authors.initials: L
authors.lastname: Aguilar
authors.forename: Jose
authors.initials: J
authors.lastname: Yuste
mesh_terms: D000209:Acute-Phase Proteins / Q000378:metabolism; D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology*; D000906:Antibodies / Q000737:chemistry*; D002443:Ceftriaxone / Q000494:pharmacology*; D002511:Cephalosporins / Q000494:pharmacology*; D003167:Complement Activation; D015922:Complement C1q / Q000737:chemistry; D015932:Complement C3c / Q000737:chemistry; D004352:Drug Resistance, Microbial; D004533:Egtazic Acid / Q000737:chemistry; D005434:Flow Cytometry / Q000379:methods; D006801:Humans; D007107:Immune System; D051379:Mice; D010587:Phagocytosis; D013296:Streptococcus pneumoniae / Q000378:metabolism*; D047090:beta-Lactams / Q000378:metabolism
chemical_list: D000209:Acute-Phase Proteins; D000900:Anti-Bacterial Agents; D000906:Antibodies; D002511:Cephalosporins; D047090:beta-Lactams; D004533:Egtazic Acid; D002443:Ceftriaxone; D015922:Complement C1q; D015932:Complement C3c; C073460:cefditoren