Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P43026 (lipopolysaccharide)
62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We investigated the efficacy of amino acids 55-76 of the synthetic shrimp anti-lipopolysaccharide factor peptide (SALF(55-76) cyclic peptide), the C-terminal part of the shrimp anti-lipopolysaccharide factor. This study was conducted to elucidate the effects of the antiseptic action of this peptide. The SALF(55-76) cyclic peptide was tested against bacterial clinical isolates and showed broad-spectrum antimicrobial activity. Transmission electron microscopic (TEM) examination of SALF(55-76) cyclic peptide-treated Pseudomonas aeruginosa showed that severe swelling preceded cell death and breakage of the outer membrane; the intracellular inclusion was found to have effluxed extracellularly. When mice were treated with the SALF(55-76) cyclic peptide before bacterial challenge with P. aeruginosa, the peptide highly protected mice against death by sepsis. The P. aeruginosa recovered from SALF(55-76) cyclic peptide-treated mice after 4 h exhibited reduced bacterial growth similar to that recovered from vancomycin-treated mice. In addition, the syntheses of inflammatory cytokines, such as interleukin (IL)-2, IL-4, IL-10, IL-12, IL-13, interferon-gamma, and tumor necrosis factor [TNF]-alpha, were significantly upregulated 4 h after SALF(55-76) cyclic peptide treatment except for IL-4 in the liver. The expressions of Toll-like receptor 4 (Tlr4), Irf3, myd88, and Tram, were considerably elevated, but only Tlr4 existed in the spleen 4 h after SALF(55-76) cyclic peptide treatment. The prophylactic administration of SALF(55-76) cyclic peptide was begun the TNF-alpha response in comparison to untreated mice by an ELISA analysis. Due to its multifunctional properties, the SALF(55-76) cyclic peptide may become an important prophylaxis against and therapy for bacterial infectious diseases, as well as for septic shock.
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PMID:Shrimp (Penaeus monodon) anti-lipopolysaccharide factor reduces the lethality of Pseudomonas aeruginosa sepsis in mice. 1738 16

The synthetic epinecidin-1(22-42) peptide was derived from positions 22-42 of Epinephelus coioides epinecidin-1. The synthetic SALF(55-76) cyclic peptide (csSALF(55-76)) and SALF(55-76) linear peptide (lsSALF(55-76)) contained sequences from positions 55 to 76 of the Penaeus monodon anti-lipopolysaccharide factor (ALF), respectively. We studied the in vitro activities of epinecidin-1(22-42), csSALF(55-76), and lsSALF(55-76) against Propionibacterium acnes, Candida albicans, and Trichomonas vaginalis. The minimum inhibitory concentrations (MICs) of epinecidin-1(22-42) for the test pathogen strains ranged 12.5-200 microg/ml, those of csSALF(55-76) ranged 100-200 microg/ml, and those of lsSALF(55-76) ranged 25-200 microg/ml. epinecidin-1(22-42) exhibited cytotoxicity towards P. acnes, C. albicans, and T. vaginalis (one strain of which was a metronidazole-resistant strain, while the other strain was not), suggesting that epinecidin-1 functions like a lytic peptide. Similar cytotoxicity was identified against T. vaginalis treated with the csSALF(55-76) and lsSALF(55-76) peptides. The antimicrobial activities of these peptides were confirmed by scanning electron microscopy (SEM), transmission electron microscopy (TEM), a viable cell count assay, and flow cytometric analysis. TEM and SEM examinations of T. vaginalis treated with these three peptides showed that severe swelling preceded cell death and breakage of the outer membrane, and the intracellular inclusion was found to have effluxed extracellularly. This phenomenon was also found with epinecidin-1(22-42) treatment of P. acnes and C. albicans. Our results suggest that the epinecidin-1(22-42), csSALF(55-76), and lsSALF(55-76) peptides may be good candidates for treating trichomoniasis, and epinecidin-1(22-42) may have potential as a drug supporting therapy for acne and candidiasis.
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PMID:In vitro activities of three synthetic peptides derived from epinecidin-1 and an anti-lipopolysaccharide factor against Propionibacterium acnes, Candida albicans, and Trichomonas vaginalis. 1946 37

In this study, to clarify the protective mechanism of a peptide from shrimp anti-lipopolysaccharide (LPS) factor (SALF) against endotoxin shock, we evaluated the effects of the SALF and LPS on the production and release of tumor necrosis factor (TNF)-alphain vitro using the RAW264.7 murine macrophage cell line. Stimulation by LPS induced the production of inflammatory cytokines, and the SALF was able to modulate TNF-alpha production in LPS-stimulated RAW264.7 cells. Microarray studies revealed a transcriptional profile which was assessed in the presence or absence of the SALF by a quantitative real-time polymerase chain reaction. Pretreatment with the SALF significantly downregulated the expression of nuclear factor (NF)-kappaB in the presence of LPS. In contrast, pretreatment with the SALF significantly elevated the expressions of Anp32a, CLU, and SLPI, which are considered to be immune-related genes in the presence of LPS. Inhibitor studies suggested that the SALF's modulation of LPS-induced TNF-alpha production involved a complex mechanism with mitogen-activated protein kinase kinase, calcium, and protein kinase C. The data from this study, which imply that the SALF can suppress TNF-alpha production, suggest a role for the SALF in the defense mechanism which can potentially be applied to mammals for endotoxin treatment.
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PMID:Antimicrobial peptide of an anti-lipopolysaccharide factor modulates of the inflammatory response in RAW264.7 cells. 2038 89