Role of Interleukin 1 Receptor Like 1 (ST2) in Gram-Negative and Gram-Positive Sepsis in Mice

Shock ◽  
2013 ◽  
Vol 40 (4) ◽  
pp. 290-296 ◽  
Author(s):  
Dana C. Blok ◽  
Alex F. de Vos ◽  
Sandrine Florquin ◽  
Tom van der Poll
Keyword(s):  
Interleukin 1 ◽  
Gram Positive ◽  
Gram Negative

scholarly journals Role of lipopolysaccharides and lipoteichoic acids on C-Chrysophsin-1 interactions with model Gram-positive and Gram-negative bacterial membranes

2020 ◽  
Vol 15 (3) ◽  
pp. 031007
Author(s):  
Todd E. Alexander ◽  
Ian M. Smith ◽  
Zachary W. Lipsky ◽  
Lindsay D. Lozeau ◽  
Terri A. Camesano
Keyword(s):  
Gram Positive ◽  
Gram Negative ◽  
Bacterial Membranes ◽  
Lipoteichoic Acids

scholarly journals The Recombination Genes addAB Are Not Restricted to Gram-Positive Bacteria: Genetic Analysis of the Recombination Initiation Enzymes RecF and AddAB in Rhizobium etli

2004 ◽  
Vol 186 (23) ◽  
pp. 7905-7913 ◽  
Author(s):  
Jacobo Zuñiga-Castillo ◽  
David Romero ◽  
Jaime M. Martínez-Salazar
Keyword(s):  
Recombination Frequency ◽  
Double Strand Breaks ◽  
Additive Effect ◽  
Gram Negative Bacteria ◽  
Rhizobium Etli ◽  
Gram Positive ◽  
Gram Negative ◽  
Strand Breaks ◽  
Gram Positive Bacteria

ABSTRACT Single-strand gaps (SSGs) and double-strand breaks (DSBs) are the major initiation sites for recombination. In bacteria, the SSGs are repaired by RecFOR, while the DSBs are processed by RecBCD in gram-negative bacteria and AddAB in gram-positive bacteria. Unexpectedly, instead of recBCD genes, the addAB genes were found in members of the α-proteobacteria group (gram negative). Taking Rhizobium etli as a model, the role of recF and addAB genes in homologous recombination and repair of damaged DNA was evaluated. Inactivation of either recF or addA provoked strong sensitivity to UV radiation and mitomycin C, while an additive effect was observed in the recF-addA mutant. The DSBs generated by nalidixic acid caused low viability only in the addA mutant. The recombination frequency of large and small plasmids was reduced in the recF mutant (24- and 36-fold, respectively), whereas a slight decrease (threefold) in the addA mutant was observed. Moreover, an additive effect (47- and 90-fold, respectively) was observed in the double mutant, but it was not as dramatic as that in a recA mutant. Interestingly, the frequency of deletion and Campbell-type recombination was slightly affected in either single or double mutants. These results suggest that another pathway exists that allows plasmid and Campbell-type recombination in the absence of recF and addA genes.

scholarly journals Role ofToll-Like Receptor 4 in Gram-Positive and Gram-Negative Pneumonia inMice

2004 ◽  
Vol 72 (2) ◽  
pp. 788-794 ◽  
Author(s):  
Judith Branger ◽  
Sylvia Knapp ◽  
Sebastiaan Weijer ◽  
Jaklien C. Leemans ◽  
Jennie M. Pater ◽  
...  
Keyword(s):  
Immune Response ◽  
Mutant Mice ◽  
Respiratory Pathogen ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Gram Positive ◽  
Gram Negative ◽  
High Level ◽  
Bacterial Outgrowth

ABSTRACT To determine the role of Toll-like receptor 4 (TLR4) in the immune response to pneumonia, C3H/HeJ mice (which display a mutant nonfunctional TLR4) and C3H/HeN wild-type mice were intranasally infected with either Streptococcus pneumoniae (a common gram-positive respiratory pathogen) or Klebsiella pneumoniae (a common gram-negative respiratory pathogen). In cases of pneumococcal pneumonia, TLR4 mutant mice showed a reduced survival only after infection with low-level bacterial doses, which was associated with a higher bacterial burden in their lungs 48 h postinfection. In Klebsiella pneumonia, TLR4 mutant mice demonstrated a shortened survival after infection with either a low- or a high-level bacterial dose together with an enhanced bacterial outgrowth in their lungs. These data suggest that TLR4 contributes to a protective immune response in both pneumococcal and Klebsiella pneumonia and that its role is more important in respiratory tract infection caused by the latter (gram-negative) pathogen.

Production of Interleukin-1 and Tumor Necrosis Factor by Human Peripheral Monocytes Activated by Periodontal Bacteria and Extracted Lipopolysaccharides

1988 ◽  
Vol 67 (8) ◽  
pp. 1131-1135 ◽  
Author(s):  
R.A. Lindemann ◽  
J.S. Economou ◽  
H. Rothermel
Keyword(s):  
Human Peripheral Blood ◽  
Interleukin 1 ◽  
Lipoteichoic Acid ◽  
Oral Bacteria ◽  
Threshold Concentration ◽  
Gram Negative Bacteria ◽  
Blood Monocytes ◽  
Gram Positive ◽  
Gram Negative ◽  
Periodontal Bacteria

Whole Gram-negative bacteria associated with juvenile and adult periodontitis, and their respective extracted lipopolysaccharides (LPS), were tested for the ability to activate quiescent human peripheral blood monocytes. All pathogenic Gram-negative bacteria and all LPS tested were able to induce the production of significant amounts of IL-1 and TNF, monokines known to induce osteoclastic bone resorption. Haemophilus segnis, which has not been associated with any form of periodontal disease, did not activate monocytes. Purified LPS from Actinobacillus actinomycetemcomitans Y4 was able to elicit IL-1 and TNF release at a threshold concentration of 1-10 ng/mL. To examine the mechanism whereby whole bacteria activated monocytes, we added polymixin B in culture with glutaraldehyde-fixed bacteria to bind LPS. This resulted in the abrogation of IL-1 and TNF production. To compare the effects of Gram-positive oral bacteria on monocytes, we also tested Staphylococcus epidermidis and the Gram-positive amphipathic equivalent of LPS, lipoteichoic acid (LTA) extracted from Staphylococcus aureus bacteria. Whereas whole Gram-positive bacteria had no stimulatory effect on monocytes, LTA induced IL-1 and TNF production at a concentration range equivalent to that of the LPS. These results indicate that monocytes are activated by free LPS or LPS bound to Gram-negative pathogenic periodontal bacteria to produce monokines which may contribute to the destruction of periodontal bone.

Prophylaxis of Predisposed Otitis Externa

1975 ◽  
Vol 84 (1) ◽  
pp. 16-21 ◽  
Author(s):  
Jimmie L. Hutchison ◽  
D. N. Wright
Keyword(s):  
Otitis Externa ◽  
Bacterial Flora ◽  
Water Repellent ◽  
External Ear ◽  
Ear Canal ◽  
Gram Positive ◽  
Gram Negative ◽  
Ear Canals ◽  
Therapeutic Compounds

Evaluation, in the guinea pig ear, of fourteen water repellent or therapeutic compounds has resulted in the recommended use of 360 Medical Fluid® as a prophylactic agent for those persons with a high risk of otitis externa. This compound was found to adhere well, be easy to apply and was nonirritating. Use of this material prevented adverse bacterial growth in ear canals exposed to water for up to seven days. The significance of maintaining the normal Gram positive bacterial flora in the external ear canal and the role of cerumen in maintaining a healthy meatal surface is discussed. A system for monitoring the health of the ear canal through measurement of the Gram positive/Gram negative bacterial ratio is suggested.

Comparable Evaluation of Orally Active Beta-Lactam Compounds in Ampicillin-Resistant Gram-Positive and Gram-Negative Rods: Role of Beta-Lactamases on Resistance

Chemotherapy ◽  
1988 ◽  
Vol 34 (3) ◽  
pp. 202-215 ◽  
Author(s):  
Wolfgang Cullmann ◽  
Wolfgang Dick ◽  
Michaela Stieglitz ◽  
Wolfgang Opferkuch
Keyword(s):  
Beta Lactam ◽  
Gram Positive ◽  
Gram Negative ◽  
Beta Lactamases ◽  
Orally Active

Streptococcus salivarius Promotes Mucin Putrefaction and Malodor Production by Porphyromonas gingivalis

2006 ◽  
Vol 85 (10) ◽  
pp. 910-914 ◽  
Author(s):  
N. Sterer ◽  
M. Rosenberg
Keyword(s):  
Porphyromonas Gingivalis ◽  
Potential Role ◽  
Oral Microbiota ◽  
Streptococcus Salivarius ◽  
Oral Malodor ◽  
Gram Positive ◽  
Gram Negative ◽  
Sds Page ◽  
Micro Organisms

Although the contribution of the oral microbiota to oral malodor is well-documented, the potential role of Gram-positive micro-organisms is unclear. In the current study, we tested the hypothesis that Gram-positive micro-organisms contribute to malodor production by deglycosylating oral glycoproteins, rendering them susceptible to subsequent proteolysis. To this end, we examined the effect of Streptococcus salivarius on Porphyromonas gingivalis-mediated putrefaction of a model glycoprotein (pig gastric mucin). Malodor was scored by two odor judges, and volatile sulfides were determined with the use of a sulfide monitor. Mucin degradation was followed by electrophoresis on SDS-PAGE. Results showed that the addition of S. salivarius or β-galactosidase promoted mucin degradation and concomitant malodor production. Addition of glycosidic inhibitors (p-APTG and glucose) inhibited this process. These results suggest that Gram-positive micro-organisms such as S. salivarius contribute to oral malodor production by deglycosylating salivary glycoproteins, thus exposing their protein core to further degradation by Gram-negative micro-organisms.

scholarly journals Intestinally Secreted C-Type Lectin Reg3b Attenuates Salmonellosis but Not Listeriosis in Mice

2012 ◽  
Vol 80 (3) ◽  
pp. 1115-1120 ◽  
Author(s):  
Marleen T. J. van Ampting ◽  
Linda M. P. Loonen ◽  
Arjan J. Schonewille ◽  
Irene Konings ◽  
Carolien Vink ◽  
...  
Keyword(s):  
Bacterial Infections ◽  
Salmonella Enteritidis ◽  
Ex Vivo ◽  
Protective Role ◽  
Carbohydrate Binding ◽  
Intestinal Infection ◽  
Gram Positive ◽  
Gram Negative ◽  
Content Type

The Reg3 protein family, including the human member designated pancreatitis-associated protein (PAP), consists of secreted proteins that contain a C-type lectin domain involved in carbohydrate binding. They are expressed by intestinal epithelial cells. Colonization of germ-free mice and intestinal infection with pathogens increase the expression of Reg3g and Reg3b in the murine ileum. Reg3g is directly bactericidal for Gram-positive bacteria, but the exact role of Reg3b in bacterial infections is unknown. To investigate the possible protective role of Reg3b in intestinal infection, Reg3b knockout (Reg3b−/−) mice and wild-type (WT) mice were orally infected with Gram-negativeSalmonella enteritidisor Gram-positiveListeria monocytogenes. At day 2 after oralListeriainfection and at day 4 after oralSalmonellainfection, mice were sacrificed to collect intestinal and other tissues for pathogen quantification. Protein expression of Reg3b and Reg3g was determined in intestinal mucosal scrapings of infected and noninfected mice. In addition,ex vivobinding of ileal mucosal Reg3b toListeriaandSalmonellawas investigated. Whereas recovery ofSalmonellaorListeriafrom feces of Reg3b−/−mice did not differ from that from feces of WT mice, significantly higher numbers of viableSalmonella, but notListeria, bacteria were recovered from the colon, mesenteric lymph nodes, spleen, and liver of the Reg3b−/−mice than from those of WT mice. Mucosal Reg3b binds to both bacterial pathogens and may interfere with their mode of action. Reg3b plays a protective role against intestinal translocation of the Gram-negative bacteriumS. enteritidisin mice but not against the Gram-positive bacteriumL. monocytogenes.

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