Differential regulation of Th1/Th2 in relevant tissues for sepsis pathogenesis with a Limulus anti-LPS factor-derived peptide increases survival in Gram-positive sepsis

Vallespí, Maribel G.; Colas, Murielle; Garay, Hilda; Reyes, Osvaldo; Araña, M.J.

doi:10.1016/j.intimp.2004.05.019

Cited by 16 publications

(15 citation statements)

References 25 publications

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“…The procedures of the cytokine assay followed the protocols of Vallespi et al [22,23] and mouse infection study section with no modifications.…”

Section: Cytokine Assaymentioning

confidence: 99%

“…It has been shown that LALFs are effective inhibitors for decreasing mortality before and after administration of LPS challenge in rabbits [21]. Reports have been published on the protective action against Pseudomonas aeruginosa and Staphylococcus haemolyticus by LALF which increased mouse survival in sepsis [22,23]. However, no detailed investigation of shrimp (P. monodon) anti-lipopolysaccharide factors (SALFs), e.g., their localization, neutralization ability, antimicrobial activity, reduction in lethality in sepsis, or cytokine gene expression patterns, has been reported.…”

Section: Introductionmentioning

confidence: 99%

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Shrimp (Penaeus monodon) anti-lipopolysaccharide factor reduces the lethality of Pseudomonas aeruginosa sepsis in mice

Pan¹,

Chao²,

Chen³

et al. 2007

International Immunopharmacology

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“…The procedures of the cytokine assay followed the protocols of Vallespi et al [22,23] and mouse infection study section with no modifications.…”

Section: Cytokine Assaymentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Shrimp (Penaeus monodon) anti-lipopolysaccharide factor reduces the lethality of Pseudomonas aeruginosa sepsis in mice

Pan¹,

Chao²,

Chen³

et al. 2007

International Immunopharmacology

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“…Thus, LALF 32–51 peptide, rather than abolishing particular cytokine(s), modulates or balances the immune response during a gram-negative sepsis. This effect acts to reduce lung damage as well as the systemic and local (lung and liver) inflammatory response [85]. In addition, the pretreatment with the peptide diminishes the particles of bacteria in the liver and increases the phagocytic activity of macrophages [85].…”

Section: Inhibition Neutralization and Clearance Of Endotoxinmentioning

confidence: 99%

“…This effect acts to reduce lung damage as well as the systemic and local (lung and liver) inflammatory response [85]. In addition, the pretreatment with the peptide diminishes the particles of bacteria in the liver and increases the phagocytic activity of macrophages [85]. Recently, cyclic cationic antimicrobial peptides of different length, based on the LALF, were synthesized [86].…”

Section: Inhibition Neutralization and Clearance Of Endotoxinmentioning

confidence: 99%

Inflammation – A New Therapeutic Target in Pneumonia

Cazzola

Matera²,

Pezzuto

2005

Respiration

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Inflammation is a hallmark of pneumonia. Therefore, managing inflammation is an attractive adjunct to targeted antibiotic therapy, mainly in severe pneumonia. Recent investigations indicate that glucocorticoids given in physiological doses (from 10-fold to 100-fold less than doses administered in the past) could be of benefit. We could also manage inflammation by administering or influencing cytokines. A major concern is that drugs designed to target a single cytokine or receptor could prove ineffective due to the redundancy of signaling pathways involved. This may require selection of drugs with broad activity or the targeting of molecules common to inflammatory signaling pathways. Drugs affecting multiple molecules or key inflammatory pathway intermediates could be more effective, but their use will need to be weighed against the risk of impairing innate immunity. Indirect approaches to manage inflammation, such as neutralizing cytotoxic substances in the lung (e.g., inhibiting, neutralizing and eliminating endotoxin), could be used in combination with other approaches. Ideally, potential treatment of life-threatening bacterial pneumonia will combine immunoadjuvant and conventional antibiotic therapy, although intense clinical research with immunotherapy has not yet yielded a successful treatment adjunct. We believe that compounds capable of stimulating early host defense and microbial clearance, but not the later phases of inflammatory tissue injury associated with sepsis, may be advantageous.

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“…For example, polymyxin B (9,10), bactericidal/permeability-increasing protein (11)(12)(13), , and mastoparan peptide (18) exhibit robust LPS-neutralizing activity in vitro and protection against lethal endotoxin shock in mouse models. Another HDP, the Limulus anti-LPS factor (LALF), which is a small basic protein from the arthropods Tachypleus tridentatus and Limulus polyphemus, is particularly attractive because it inhibits the endotoxin-mediated activation of the coagulation cascade by binding to LPS (19,20). We previously characterized the core domain of LPS binding in LALF (amino acids 31-52) (21) and used this sequence to generate a novel peptide, CLP-19, with optimized anti-LPS activity.…”

mentioning

confidence: 99%

Looped Host Defense Peptide CLP-19 Binds to Microtubules and Inhibits Surface Expression of TLR4 on Mouse Macrophages

Liu

Yang

et al. 2013

The Journal of Immunology

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The looped host defense peptide CLP-19 is derived from a highly functional core region of the Limulus anti-LPS factor and exerts robust anti-LPS activity by directly interacting with LPS in the extracellular space. We previously showed that prophylactic administration of CLP-19 even 20 h prior to LPS challenge might significantly increase the survival rate in a lethal endotoxin shock mouse model. Such an effect may be associated with immune regulation of CLP-19. To investigate the underlying mechanisms, peptide affinity chromatography, immunofluorescence, and Western blotting procedures were used to identify α- and β-tubulin as direct and specific binding partners of CLP-19 in the mouse macrophage cell line RAW 264.7. Bioinformatic analysis using the AutoDock Vina molecular docking and PyMOL molecular graphics system predicted that CLP-19 would bind to the functional residues of both α- and β-tubulin and would be located within the groove of microtubules. Tubulin polymerization assay revealed that CLP-19 might induce polymerization of microtubules and prevent depolymerization. The immunoregulatory effect of CLP-19 involving microtubules was investigated by flow cytometry, immunofluorescence, and Western blotting, which showed that CLP-19 prophylactic treatment of RAW 264.7 cells significantly inhibited LPS-induced surface expression of TLR4. Taken together, these results suggest that CLP-19 binding to microtubules disrupts the dynamic equilibrium of microtubules, reducing the efficacy of microtubule-dependent vesicular transport that would otherwise translocate TLR4 from the endoplasmic reticulum to the cell surface.

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Differential regulation of Th1/Th2 in relevant tissues for sepsis pathogenesis with a Limulus anti-LPS factor-derived peptide increases survival in Gram-positive sepsis

Cited by 16 publications

References 25 publications

Shrimp (Penaeus monodon) anti-lipopolysaccharide factor reduces the lethality of Pseudomonas aeruginosa sepsis in mice

Shrimp (Penaeus monodon) anti-lipopolysaccharide factor reduces the lethality of Pseudomonas aeruginosa sepsis in mice

Inflammation – A New Therapeutic Target in Pneumonia

Looped Host Defense Peptide CLP-19 Binds to Microtubules and Inhibits Surface Expression of TLR4 on Mouse Macrophages

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