Group B Streptococci Exposed to Rifampin or Clindamycin (versus Ampicillin or Cefotaxime) Stimulate Reduced Production of Inflammatory Mediators by Murine Macrophages

Brinkmann, K C; Talati, Ajay J.; Akbari, Raumina E; Meals, Elizabeth; English, B. Keith

doi:10.1203/01.pdr.0000153946.97159.79

Cited by 19 publications

(14 citation statements)

References 29 publications

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“…In in vitro experiments, the release of LTA/teichoic acid during the treatment of S. pneumoniae infections with different antibiotics that inhibit bacterial protein synthesis (ri-fampin, rifabutin, quinupristin-dalfopristin, or clindamycin) was attenuated compared to that observed when ceftriaxone or meropenem treatment was used (16,31,50). Similarly, group B streptococci exposed to rifampin or clindamycin (as opposed to ampicillin or cefotaxime) reduced the levels of production of inflammatory mediators by murine macrophages upon stimulation (6). In an experimental model of meningitis, the use of clindamycin, rifampin, and quinupristin-dalfopristin has also been proven to be beneficial in terms of LTA release, neurological damage, and/or mortality (5,13,39,51).…”

Section: Discussionmentioning

confidence: 99%

Prevention of Brain Injury by the Nonbacteriolytic Antibiotic Daptomycin in Experimental Pneumococcal Meningitis

Grandgirard

Schürch

Cottagnoud³

et al. 2007

Antimicrob Agents Chemother

102

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Bacteriolytic antibiotics cause the release of bacterial components that augment the host inflammatory response, which in turn contributes to the pathophysiology of brain injury in bacterial meningitis. In the present study, antibiotic therapy with nonbacteriolytic daptomycin was compared with that of bacteriolytic ceftriaxone in experimental pneumococcal meningitis, and the treatments were evaluated for their effects on inflammation and brain injury. Eleven-day-old rats were injected intracisternally with 1.3 ؋ 10 4 ؎ 0.5 ؋ 10 4 CFU of Streptococcus pneumoniae serotype 3 and randomized to therapy with ceftriaxone (100 mg/kg of body weight subcutaneously [s.c.]; n ‫؍‬ 55) or daptomycin (50 mg/kg s.c.; n ‫؍‬ 56) starting at 18 h after infection. The cerebrospinal fluid (CSF) was assessed for bacterial counts, matrix metalloproteinase-9 levels, and tumor necrosis factor alpha levels at different time intervals after infection. Cortical brain damage was evaluated at 40 h after infection. Daptomycin cleared the bacteria more efficiently from the CSF than ceftriaxone within 2 h after the initiation of therapy (log 10 3.6 ؎ 1.0 and log 10 6.3 ؎ 1.4 CFU/ml, respectively; P < 0.02); reduced the inflammatory host reaction, as assessed by the matrix metalloproteinase-9 concentration in CSF 40 h after infection (P < 0.005); and prevented the development of cortical injury (cortical injury present in 0/30 and 7/28 animals, respectively; P < 0.004). Compared to ceftriaxone, daptomycin cleared the bacteria from the CSF more rapidly and caused less CSF inflammation. This combined effect provides an explanation for the observation that daptomycin prevented the development of cortical brain injury in experimental pneumococcal meningitis. Further research is needed to investigate whether nonbacteriolytic antibiotic therapy with daptomycin represents an advantageous alternative over current bacteriolytic antibiotic therapies for the treatment of pneumococcal meningitis.

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Section: Discussionmentioning

confidence: 99%

Prevention of Brain Injury by the Nonbacteriolytic Antibiotic Daptomycin in Experimental Pneumococcal Meningitis

Grandgirard

Schürch

Cottagnoud³

et al. 2007

Antimicrob Agents Chemother

102

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“…Experiments were done in 6-well tissue culture plates (Becton Dickinson, Lincoln Park, NJ) with 4 ϫ 10 6 to 4.7 ϫ 10 6 cells/well or in 24-well tissue culture plates with 1 ϫ 10 6 cells/well. An antibiotic(s) was added to the cell cultures immediately before the addition of live staphylococci (10 5 to 10 7 CFU/ml); then cells were incubated for 18 h. In studies of iNOS protein accumulation, low concentrations of recombinant gamma interferon (rIFN-␥) (Sigma, St. Louis, MO) were added (3,14).…”

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confidence: 99%

“…Unpaired twotailed t tests were used to compare TNF secretion by cells stimulated with each bacterial isolate in the presence of different antibiotics (a P value of Ͻ0.05 was considered significant). Cell lysates were prepared as described previously (3,14) and were analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, transferred to nitrocellulose membranes, and reacted with a murine monoclonal antibody specific for iNOS (Transduction Laboratories, Lexington, KY) followed by a sheep anti-mouse immunoglobulin G peroxidase-linked conjugate (Amersham, Arlington Heights, IL). iNOS protein was detected by enhanced chemiluminescence (Amersham), and band intensities were quantitated using a Bio-Rad model GS-700 densitometer.…”

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confidence: 99%

Diminished Macrophage Inflammatory Response to Staphylococcus aureus Isolates Exposed to Daptomycin versus Vancomycin or Oxacillin

English¹,

Maryniw

Talati

et al. 2006

Antimicrob Agents Chemother

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“…They encourage epidemiological studies on a possible link between MS onset or exacerbation and infections with S. pneumoniae. Whether the detrimental effect of bacterial infections on the course of EAE can be attenuated by antibiotic therapy tailored to minimize the release of proinflammatory bacterial products (3,39,45) remains to be studied. …”

Section: Fig 7 Costimulatory Molecules On Cd11cmentioning

confidence: 99%

“…TLRs recognize specific patterns of microbial components and regulate the activation of both innate and adaptive immunity (28,40). The quantity of TLR agonists released by bacteria is influenced by the mode of antibiotic treatment (3,39,45).…”

mentioning

confidence: 99%

Streptococcus pneumoniaeInfection Aggravates Experimental Autoimmune Encephalomyelitis via Toll-Like Receptor 2

et al. 2006

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The course of autoimmune inflammatory diseases of the central nervous system (CNS) can be influenced by infections. Here we assessed the disease-modulating effects of the most frequent respiratory pathogen Streptococcus pneumonia on the course of experimental autoimmune encephalomyelitis (EAE). Mice were immunized with myelin oligodendrocyte glycoprotein 35-55 (MOG 35-55 ) peptide, challenged intraperitoneally with live S. pneumoniae type 3, and then treated with ceftriaxone. EAE was monitored by a clinical score for 35 days after immunization. EAE was unaltered in mice infected with S. pneumoniae 2 days before and 21 days after the first MOG 35-55 injection but was more severe in animals infected 7 days after the first MOG 35-55 injection. The antigen-driven systemic T-cell response was unaltered, and the intraspinal Th1 cytokine mRNA concentrations at the peak of disease were unchanged. The composition of CNS-infiltrating cells and subsequent tissue destruction were only slightly increased after S. pneumoniae infection. In contrast, the serum levels of tumor necrosis factor alpha and interleukin-6 and spinal interleukin-6 levels were elevated, and the expression of major histocompatibility complex class II molecules, CD80, and CD86 on splenic dendritic cells were enhanced early after infection. Serum cytokine concentrations were not elevated, and EAE was not aggravated by S. pneumoniae infection in Toll-like receptor 2 (TLR2)-deficient mice. In conclusion, infection with S. pneumoniae worsens EAE probably by elevation of proinflammatory cytokines and activation of dendritic cells in the systemic circulation via TLR2 and cross talk through the blood-brain barrier.

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Group B Streptococci Exposed to Rifampin or Clindamycin (versus Ampicillin or Cefotaxime) Stimulate Reduced Production of Inflammatory Mediators by Murine Macrophages

Cited by 19 publications

References 29 publications

Prevention of Brain Injury by the Nonbacteriolytic Antibiotic Daptomycin in Experimental Pneumococcal Meningitis

Prevention of Brain Injury by the Nonbacteriolytic Antibiotic Daptomycin in Experimental Pneumococcal Meningitis

Diminished Macrophage Inflammatory Response to Staphylococcus aureus Isolates Exposed to Daptomycin versus Vancomycin or Oxacillin

Streptococcus pneumoniaeInfection Aggravates Experimental Autoimmune Encephalomyelitis via Toll-Like Receptor 2

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