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Gram-positive bacteria

About: Gram-positive bacteria is a research topic. Over the lifetime, 3031 publications have been published within this topic receiving 81155 citations. The topic is also known as: Gram-positive.


Papers
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Journal ArticleDOI
01 Oct 1999-Immunity
TL;DR: It is demonstrated that TLR2 and TLR4 recognize different bacterial cell wall components in vivo andTLR2 plays a major role in Gram-positive bacterial recognition.

3,364 citations

Journal ArticleDOI
TL;DR: Antibacterial activities of chitosan was inversely affected by pH (pH 4.5-5.9 range tested), with higher activity at lower pH value, and bactericidal effects with gram-positive bacteria than gram-negative bacteria in the presence of 0.1% chitOSan.

1,382 citations

Journal Article
TL;DR: The similarity of clinical response to invasive infection by Gram-positive and Gram-negative bacteria is due to bacterial recognition via similar TLRs, and a soluble preparation of peptidoglycan prepared from S. aureus was tested.
Abstract: Invasive infection with Gram-positive and Gram-negative bacteria often results in septic shock and death. The basis for the earliest steps in innate immune response to Gram-positive bacterial infection is poorly understood. The LPS component of the Gram-negative bacterial cell wall appears to activate cells via CD14 and Toll-like receptor (TLR) 2 and TLR4. We hypothesized that Gram-positive bacteria might also be recognized by TLRs. Heterologous expression of human TLR2, but not TLR4, in fibroblasts conferred responsiveness to Staphylococcus aureus and Streptococcus pneumoniae as evidenced by inducible translocation of NF-kappaB. CD14 coexpression synergistically enhanced TLR2-mediated activation. To determine which components of Gram-positive cell walls activate Toll proteins, we tested a soluble preparation of peptidoglycan prepared from S. aureus. Soluble peptidoglycan substituted for whole organisms. These data suggest that the similarity of clinical response to invasive infection by Gram-positive and Gram-negative bacteria is due to bacterial recognition via similar TLRs.

1,291 citations

Journal ArticleDOI
TL;DR: The most common mechanisms that help Gram-positive bacteria overcome the challenge posed by different acidic environments are described, i.e., the use of proton pumps, the protection or repair of macromolecules, cell membrane changes, production of alkali, induction of pathways by transcriptional regulators, alteration of metabolism, and the role of cell density and cell signaling.
Abstract: Gram-positive bacteria possess a myriad of acid resistance systems that can help them to overcome the challenge posed by different acidic environments. In this review the most common mechanisms are described: i.e., the use of proton pumps, the protection or repair of macromolecules, cell membrane changes, production of alkali, induction of pathways by transcriptional regulators, alteration of metabolism, and the role of cell density and cell signaling. We also discuss the reponses of Listeria monocytogenes, Rhodococcus, Mycobacterium, Clostridium perfringens, Staphylococcus aureus, Bacillus cereus, oral streptococci, and lactic acid bacteria to acidic environments and outline ways in which this knowledge has been or may be used to either aid or prevent bacterial survival in low-pH environments.

1,114 citations

Journal ArticleDOI
TL;DR: A new antibacterial substance, designated as streptomycin, was isolated from two strains of an actinomyces related to an organism described as Actinomycles griseus, which resembles streptothricin in its solubility in water, mode of isolation and concentration from culture medium, its selective activity against gram-negative bacteria, and its limited toxicity to animals.
Abstract: SummaryA new antibacterial substance, designated as streptomycin, was isolated from two strains of an actinomyces related to an organism described as Actinomyces griseus. This substance resembles s...

955 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202337
202299
202157
202099
201994
201898