Supernatants from Staphylococcus epidermidis grown in the presence of different antibiotics induce differential release of tumor necrosis factor alpha from human monocytes.
Journal: 1996/November - Infection and Immunity
ISSN: 0019-9567
PUBMED: 8926110
Abstract:
Bacterial products from gram-positive bacteria, such as peptidoglycan, teichoic acid, and toxins, activate mononuclear cells to produce tumor necrosis factor alpha (TNF). The present study evaluated the release of soluble cell wall components from Staphylococcus epidermidis capable of inducing TNF after exposure of the bacteria to various antibiotics. A clinical S. epidermidis isolate (694) was incubated with either penicillin, oxacillin, vancomycin, or clindamycin at five times the MIC. Supernatants of the cultures obtained by filtration were added to plastic adherent monocytes in the absence or presence of human serum. After 18 h of incubation, monocyte supernatants were tested for the presence of TNF by enzyme-linked immunosorbent assay (ELISA). Supernatants from bacteria incubated with beta-lactam antibiotics induced higher TNF levels than those obtained from bacteria incubated with culture medium only (no antibiotics), vancomycin, or clindamycin. Human serum potentiated supernatant-induced TNF release, especially in beta-lactam supernatants. The soluble peptidoglycan and teichoic acid contents of supernatants, as estimated by inhibition ELISA and, for peptidoglycan, also by affinity depletion with vancomycin-Sepharose gel, were proportional to TNF release. Differences in the ability of individual antibiotics to generate TNF-releasing products from S. epidermidis were observed, the most potent antibiotics being penicillin and oxacillin.
Relations:
Content
Citations
(7)
References
(36)
Drugs
(6)
Chemicals
(5)
Organisms
(2)
Anatomy
(1)
Similar articles
Articles by the same authors
Discussion board
Infect Immun 64(10): 4351-4355

Supernatants from Staphylococcus epidermidis grown in the presence of different antibiotics induce differential release of tumor necrosis factor alpha from human monocytes.

Abstract

Bacterial products from gram-positive bacteria, such as peptidoglycan, teichoic acid, and toxins, activate mononuclear cells to produce tumor necrosis factor alpha (TNF). The present study evaluated the release of soluble cell wall components from Staphylococcus epidermidis capable of inducing TNF after exposure of the bacteria to various antibiotics. A clinical S. epidermidis isolate (694) was incubated with either penicillin, oxacillin, vancomycin, or clindamycin at five times the MIC. Supernatants of the cultures obtained by filtration were added to plastic adherent monocytes in the absence or presence of human serum. After 18 h of incubation, monocyte supernatants were tested for the presence of TNF by enzyme-linked immunosorbent assay (ELISA). Supernatants from bacteria incubated with beta-lactam antibiotics induced higher TNF levels than those obtained from bacteria incubated with culture medium only (no antibiotics), vancomycin, or clindamycin. Human serum potentiated supernatant-induced TNF release, especially in beta-lactam supernatants. The soluble peptidoglycan and teichoic acid contents of supernatants, as estimated by inhibition ELISA and, for peptidoglycan, also by affinity depletion with vancomycin-Sepharose gel, were proportional to TNF release. Differences in the ability of individual antibiotics to generate TNF-releasing products from S. epidermidis were observed, the most potent antibiotics being penicillin and oxacillin.

Full Text

The Full Text of this article is available as a PDF (223K).

Selected References

These references are in PubMed. This may not be the complete list of references from this article.
  • Bhakdi S, Klonisch T, Nuber P, Fischer W. Stimulation of monokine production by lipoteichoic acids. Infect Immun. 1991 Dec;59(12):4614–4620.[PMC free article] [PubMed] [Google Scholar]
  • Bhakdi S, Muhly M, Korom S, Hugo F. Release of interleukin-1 beta associated with potent cytocidal action of staphylococcal alpha-toxin on human monocytes. Infect Immun. 1989 Nov;57(11):3512–3519.[PMC free article] [PubMed] [Google Scholar]
  • Bone RC. The pathogenesis of sepsis. Ann Intern Med. 1991 Sep 15;115(6):457–469. [PubMed] [Google Scholar]
  • Böyum A. Isolation of mononuclear cells and granulocytes from human blood. Isolation of monuclear cells by one centrifugation, and of granulocytes by combining centrifugation and sedimentation at 1 g. Scand J Clin Lab Invest Suppl. 1968;97:77–89. [PubMed] [Google Scholar]
  • Burchard KW, Minor LB, Slotman GJ, Gann DS. Staphylococcus epidermidis sepsis in surgical patients. Arch Surg. 1984 Jan;119(1):96–100. [PubMed] [Google Scholar]
  • Crowder JG, White A. Teichoic acid antibodies in staphylococcal and nonstaphylococcal endocarditis. Ann Intern Med. 1972 Jul;77(1):87–90. [PubMed] [Google Scholar]
  • Eykyn SJ. Staphylococcal sepsis. The changing pattern of disease and therapy. Lancet. 1988 Jan 16;1(8577):100–104. [PubMed] [Google Scholar]
  • Gemmell CG, Thelestam M. Toxinogenicity of clinical isolates of coagulase-negative staphylococci towards various animal cells. Acta Pathol Microbiol Scand B. 1981 Dec;89(6):417–421. [PubMed] [Google Scholar]
  • Gold MR, Miller CL, Mishell RI. Soluble non-cross-linked peptidoglycan polymers stimulate monocyte-macrophage inflammatory functions. Infect Immun. 1985 Sep;49(3):731–741.[PMC free article] [PubMed] [Google Scholar]
  • Goldberg ME, Djavadi-Ohaniance L. Methods for measurement of antibody/antigen affinity based on ELISA and RIA. Curr Opin Immunol. 1993 Apr;5(2):278–281. [PubMed] [Google Scholar]
  • Heumann D, Barras C, Severin A, Glauser MP, Tomasz A. Gram-positive cell walls stimulate synthesis of tumor necrosis factor alpha and interleukin-6 by human monocytes. Infect Immun. 1994 Jul;62(7):2715–2721.[PMC free article] [PubMed] [Google Scholar]
  • Issekutz AC. Removal of gram-negative endotoxin from solutions by affinity chromatography. J Immunol Methods. 1983 Jul 29;61(3):275–281. [PubMed] [Google Scholar]
  • Kernodle DS, McGraw PA, Barg NL, Menzies BE, Voladri RK, Harshman S. Growth of Staphylococcus aureus with nafcillin in vitro induces alpha-toxin production and increases the lethal activity of sterile broth filtrates in a murine model. J Infect Dis. 1995 Aug;172(2):410–419. [PubMed] [Google Scholar]
  • Leeson MC, Fujihara Y, Morrison DC. Evidence for lipopolysaccharide as the predominant proinflammatory mediator in supernatants of antibiotic-treated bacteria. Infect Immun. 1994 Nov;62(11):4975–4980.[PMC free article] [PubMed] [Google Scholar]
  • Martin MA, Pfaller MA, Wenzel RP. Coagulase-negative staphylococcal bacteremia. Mortality and hospital stay. Ann Intern Med. 1989 Jan 1;110(1):9–16. [PubMed] [Google Scholar]
  • Mattsson E, Rollof J, Verhoef J, Van Dijk H, Fleer A. Serum-induced potentiation of tumor necrosis factor alpha production by human monocytes in response to staphylococcal peptidoglycan: involvement of different serum factors. Infect Immun. 1994 Sep;62(9):3837–3843.[PMC free article] [PubMed] [Google Scholar]
  • Mattsson E, Van Dijk H, Van Kessel K, Verhoef J, Fleer A, Rollof J. Intracellular pathways involved in tumor necrosis factor-alpha release by human monocytes on stimulation with lipopolysaccharide or staphylococcal peptidoglycan are partly similar. J Infect Dis. 1996 Jan;173(1):212–218. [PubMed] [Google Scholar]
  • Mattsson E, Verhage L, Rollof J, Fleer A, Verhoef J, van Dijk H. Peptidoglycan and teichoic acid from Staphylococcus epidermidis stimulate human monocytes to release tumour necrosis factor-alpha, interleukin-1 beta and interleukin-6. FEMS Immunol Med Microbiol. 1993 Oct;7(3):281–287. [PubMed] [Google Scholar]
  • Mirelman D, Bracha R, Sharon N. Penicillin-induced secretion of soluble, uncross-linked peptidoglycan by Micrococcus luteus cells. Biochemistry. 1974 Nov 19;13(24):5045–5053. [PubMed] [Google Scholar]
  • Parsonnet J, Gillis ZA. Production of tumor necrosis factor by human monocytes in response to toxic-shock-syndrome toxin-1. J Infect Dis. 1988 Nov;158(5):1026–1033. [PubMed] [Google Scholar]
  • Peterson PK, Wilkinson BJ, Kim Y, Schmeling D, Douglas SD, Quie PG, Verhoef J. The key role of peptidoglycan in the opsonization of Staphylococcus aureus. J Clin Invest. 1978 Mar;61(3):597–609.[PMC free article] [PubMed] [Google Scholar]
  • Pfeffer K, Matsuyama T, Kündig TM, Wakeham A, Kishihara K, Shahinian A, Wiegmann K, Ohashi PS, Krönke M, Mak TW. Mice deficient for the 55 kd tumor necrosis factor receptor are resistant to endotoxic shock, yet succumb to L. monocytogenes infection. Cell. 1993 May 7;73(3):457–467. [PubMed] [Google Scholar]
  • Ponce de Leon S, Wenzel RP. Hospital-acquired bloodstream infections with Staphylococcus epidermidis. Review of 100 cases. Am J Med. 1984 Oct;77(4):639–644. [PubMed] [Google Scholar]
  • Prins JM, Kuijper EJ, Mevissen ML, Speelman P, van Deventer SJ. Release of tumor necrosis factor alpha and interleukin 6 during antibiotic killing of Escherichia coli in whole blood: influence of antibiotic class, antibiotic concentration, and presence of septic serum. Infect Immun. 1995 Jun;63(6):2236–2242.[PMC free article] [PubMed] [Google Scholar]
  • Rabin RL, Bieber MM, Teng NN. Lipopolysaccharide and peptidoglycan share binding sites on human peripheral blood monocytes. J Infect Dis. 1993 Jul;168(1):135–142. [PubMed] [Google Scholar]
  • Raynor RH, Scott DF, Best GK. Oxacillin-induced lysis of Staphylococcus aureus. Antimicrob Agents Chemother. 1979 Aug;16(2):134–140.[PMC free article] [PubMed] [Google Scholar]
  • Rotta J. Endotoxin-like properties of the peptidoglycan. Z Immunitatsforsch Exp Klin Immunol. 1975 Jul;149(2-4):230–244. [PubMed] [Google Scholar]
  • Simon DM, Koenig G, Trenholme GM. Differences in release of tumor necrosis factor from THP-1 cells stimulated by filtrates of antibiotic-killed Escherichia coli. J Infect Dis. 1991 Oct;164(4):800–802. [PubMed] [Google Scholar]
  • Tracey KJ, Lowry SF, Cerami A. Cachectin: a hormone that triggers acute shock and chronic cachexia. J Infect Dis. 1988 Mar;157(3):413–420. [PubMed] [Google Scholar]
  • Vaudaux P, Grau GE, Huggler E, Schumacher-Perdreau F, Fiedler F, Waldvogel FA, Lew DP. Contribution of tumor necrosis factor to host defense against staphylococci in a guinea pig model of foreign body infections. J Infect Dis. 1992 Jul;166(1):58–64. [PubMed] [Google Scholar]
  • Wakabayashi G, Gelfand JA, Jung WK, Connolly RJ, Burke JF, Dinarello CA. Staphylococcus epidermidis induces complement activation, tumor necrosis factor and interleukin-1, a shock-like state and tissue injury in rabbits without endotoxemia. Comparison to Escherichia coli. J Clin Invest. 1991 Jun;87(6):1925–1935.[PMC free article] [PubMed] [Google Scholar]
  • Wecke J, Johannsen L, Giesbrecht P. Reduction of wall degradability of clindamycin-treated staphylococci within macrophages. Infect Immun. 1990 Jan;58(1):197–204.[PMC free article] [PubMed] [Google Scholar]
  • Weidemann B, Brade H, Rietschel ET, Dziarski R, Bazil V, Kusumoto S, Flad HD, Ulmer AJ. Soluble peptidoglycan-induced monokine production can be blocked by anti-CD14 monoclonal antibodies and by lipid A partial structures. Infect Immun. 1994 Nov;62(11):4709–4715.[PMC free article] [PubMed] [Google Scholar]
  • Wheat LJ, Wilkinson BJ, Kohler RB, White AC. Antibody response to peptidoglycan during staphylococcal infections. J Infect Dis. 1983 Jan;147(1):16–22. [PubMed] [Google Scholar]
  • Zeiger AR, Tuazon CU, Sheagren JN. Antibody levels to bacterial peptidoglycan in human sera during the time course of endocarditis and bacteremic infections caused by Staphylococcus aureus. Infect Immun. 1981 Sep;33(3):795–800.[PMC free article] [PubMed] [Google Scholar]
  • Zeiger AR, Wong W, Chatterjee AN, Young FE, Tuazon CU. Evidence for the secretion of soluble peptidoglycans by clinical isolates of Staphylococcus aureus. Infect Immun. 1982 Sep;37(3):1112–1118.[PMC free article] [PubMed] [Google Scholar]
Eijkman-Winkler Institute for Medical Microbiology, Infectious Diseases, and Inflammation, Utrecht, The Netherlands.
Eijkman-Winkler Institute for Medical Microbiology, Infectious Diseases, and Inflammation, Utrecht, The Netherlands.

Abstract

Bacterial products from gram-positive bacteria, such as peptidoglycan, teichoic acid, and toxins, activate mononuclear cells to produce tumor necrosis factor alpha (TNF). The present study evaluated the release of soluble cell wall components from Staphylococcus epidermidis capable of inducing TNF after exposure of the bacteria to various antibiotics. A clinical S. epidermidis isolate (694) was incubated with either penicillin, oxacillin, vancomycin, or clindamycin at five times the MIC. Supernatants of the cultures obtained by filtration were added to plastic adherent monocytes in the absence or presence of human serum. After 18 h of incubation, monocyte supernatants were tested for the presence of TNF by enzyme-linked immunosorbent assay (ELISA). Supernatants from bacteria incubated with beta-lactam antibiotics induced higher TNF levels than those obtained from bacteria incubated with culture medium only (no antibiotics), vancomycin, or clindamycin. Human serum potentiated supernatant-induced TNF release, especially in beta-lactam supernatants. The soluble peptidoglycan and teichoic acid contents of supernatants, as estimated by inhibition ELISA and, for peptidoglycan, also by affinity depletion with vancomycin-Sepharose gel, were proportional to TNF release. Differences in the ability of individual antibiotics to generate TNF-releasing products from S. epidermidis were observed, the most potent antibiotics being penicillin and oxacillin.

Abstract
Full Text
Selected References
Collaboration tool especially designed for Life Science professionals.Drag-and-drop any entity to your messages.