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Lipid isolated from a Leishmania donovani strain reduces Escherichia coli induced sepsis in mice through inhibition of inflammatory responses.

Das S, Chatterjee N, Bose D, Banerjee S, Pal P, Jha T, Das Saha K - Mediators Inflamm. (2014)

Bottom Line: Due to the effect of LTL, E. coli induced inflammatory cytokine-chemokine(s) levels were significantly reduced in serum and bronchoalveolar lavage fluid simultaneously.LTL also improved the lung injury and suppressed the cell adhesion molecules in lung tissue.These findings indicate that LTL may prove to be a potential anti-inflammatory agent and provide protection against gram-negative bacterial sepsis with pulmonary impairment.

View Article: PubMed Central - PubMed

Affiliation: Cancer Biology & Inflammatory Disorder Division, CSIR-Indian Institute of Chemical Biology, 4 Raja S.C. Mullick Road, Kolkata, West Bengal 700032, India.

ABSTRACT
Sepsis is the reflection of systemic immune response that manifests in the sequential inflammatory process in presence of infection. This may occur as a result of gram-negative bacterial sepsis including Escherichia coli infection that gives rise to excessive production of inflammatory mediators and causes severe tissue injuries. We have reported earlier that the lipid of attenuated Leishmania donovani suppresses the inflammatory responses in arthritis patients. Using heat killed E. coli stimulated macrophages, we have now investigated the effect of leishmanial total lipid (LTL) isolated from Leishmania donovani (MHO/IN/1978/UR6) for amelioration of the inflammatory mediators and transcriptional factor with suppression of TLR4-CD14 expression. To evaluate the in vivo effect, E. coli induced murine sepsis model was used focusing on the changes in different parameter(s) of lung injury caused by sepsis, namely, edema, vascular permeability, and pathophysiology, and the status of different cytokine-chemokine(s) and adhesion molecule(s). Due to the effect of LTL, E. coli induced inflammatory cytokine-chemokine(s) levels were significantly reduced in serum and bronchoalveolar lavage fluid simultaneously. LTL also improved the lung injury and suppressed the cell adhesion molecules in lung tissue. These findings indicate that LTL may prove to be a potential anti-inflammatory agent and provide protection against gram-negative bacterial sepsis with pulmonary impairment.

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Related in: MedlinePlus

Effect of LTL in cellular localization of (a) intercellular adhesion molecule-1 (ICAM-1, green) and vascular cell adhesion molecule-1 (VACM-1, red); arrow indicates localization of cell adhesion molecule evaluated by laser scanning confocal microscope in 100x magnification. (b) Western blot protein level expression of cell adhesion; ICAM-1, VCAM-1, P-selectin, and E-selectin were markedly suppressed after E. coli O18:K1, 104 CFU challenge and pretreatment with LTL at doses LTLD1 (25 mg/kg) and LTLD2 (50 mg/kg) in mice lung.
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fig7: Effect of LTL in cellular localization of (a) intercellular adhesion molecule-1 (ICAM-1, green) and vascular cell adhesion molecule-1 (VACM-1, red); arrow indicates localization of cell adhesion molecule evaluated by laser scanning confocal microscope in 100x magnification. (b) Western blot protein level expression of cell adhesion; ICAM-1, VCAM-1, P-selectin, and E-selectin were markedly suppressed after E. coli O18:K1, 104 CFU challenge and pretreatment with LTL at doses LTLD1 (25 mg/kg) and LTLD2 (50 mg/kg) in mice lung.

Mentions: Inflammatory mediators and cell adhesion molecules including ICAM-1, VCAM-1, P-selectin, and E-selectin participate in inflammatory sepsis induced lung injury. ICAM-1 and VCAM-1 were used in our study to observe the effect of LTL on the lung of E. coli challenged mice. LTLD1 and LTLD2 were found to cause significant reduction in ICAM and VCAM-1 levels of lung epithelial tissue as compared to the only E. coli infected group (Figure 7(a)). Furthermore, western blot data revealed that upon pretreatment with LTLD1 and LTLD2, the protein level expressions of P-selectin and E-selectin were reduced at 24 h as seen in Figure 7(b).


Lipid isolated from a Leishmania donovani strain reduces Escherichia coli induced sepsis in mice through inhibition of inflammatory responses.

Das S, Chatterjee N, Bose D, Banerjee S, Pal P, Jha T, Das Saha K - Mediators Inflamm. (2014)

Effect of LTL in cellular localization of (a) intercellular adhesion molecule-1 (ICAM-1, green) and vascular cell adhesion molecule-1 (VACM-1, red); arrow indicates localization of cell adhesion molecule evaluated by laser scanning confocal microscope in 100x magnification. (b) Western blot protein level expression of cell adhesion; ICAM-1, VCAM-1, P-selectin, and E-selectin were markedly suppressed after E. coli O18:K1, 104 CFU challenge and pretreatment with LTL at doses LTLD1 (25 mg/kg) and LTLD2 (50 mg/kg) in mice lung.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4120923&req=5

fig7: Effect of LTL in cellular localization of (a) intercellular adhesion molecule-1 (ICAM-1, green) and vascular cell adhesion molecule-1 (VACM-1, red); arrow indicates localization of cell adhesion molecule evaluated by laser scanning confocal microscope in 100x magnification. (b) Western blot protein level expression of cell adhesion; ICAM-1, VCAM-1, P-selectin, and E-selectin were markedly suppressed after E. coli O18:K1, 104 CFU challenge and pretreatment with LTL at doses LTLD1 (25 mg/kg) and LTLD2 (50 mg/kg) in mice lung.
Mentions: Inflammatory mediators and cell adhesion molecules including ICAM-1, VCAM-1, P-selectin, and E-selectin participate in inflammatory sepsis induced lung injury. ICAM-1 and VCAM-1 were used in our study to observe the effect of LTL on the lung of E. coli challenged mice. LTLD1 and LTLD2 were found to cause significant reduction in ICAM and VCAM-1 levels of lung epithelial tissue as compared to the only E. coli infected group (Figure 7(a)). Furthermore, western blot data revealed that upon pretreatment with LTLD1 and LTLD2, the protein level expressions of P-selectin and E-selectin were reduced at 24 h as seen in Figure 7(b).

Bottom Line: Due to the effect of LTL, E. coli induced inflammatory cytokine-chemokine(s) levels were significantly reduced in serum and bronchoalveolar lavage fluid simultaneously.LTL also improved the lung injury and suppressed the cell adhesion molecules in lung tissue.These findings indicate that LTL may prove to be a potential anti-inflammatory agent and provide protection against gram-negative bacterial sepsis with pulmonary impairment.

View Article: PubMed Central - PubMed

Affiliation: Cancer Biology & Inflammatory Disorder Division, CSIR-Indian Institute of Chemical Biology, 4 Raja S.C. Mullick Road, Kolkata, West Bengal 700032, India.

ABSTRACT
Sepsis is the reflection of systemic immune response that manifests in the sequential inflammatory process in presence of infection. This may occur as a result of gram-negative bacterial sepsis including Escherichia coli infection that gives rise to excessive production of inflammatory mediators and causes severe tissue injuries. We have reported earlier that the lipid of attenuated Leishmania donovani suppresses the inflammatory responses in arthritis patients. Using heat killed E. coli stimulated macrophages, we have now investigated the effect of leishmanial total lipid (LTL) isolated from Leishmania donovani (MHO/IN/1978/UR6) for amelioration of the inflammatory mediators and transcriptional factor with suppression of TLR4-CD14 expression. To evaluate the in vivo effect, E. coli induced murine sepsis model was used focusing on the changes in different parameter(s) of lung injury caused by sepsis, namely, edema, vascular permeability, and pathophysiology, and the status of different cytokine-chemokine(s) and adhesion molecule(s). Due to the effect of LTL, E. coli induced inflammatory cytokine-chemokine(s) levels were significantly reduced in serum and bronchoalveolar lavage fluid simultaneously. LTL also improved the lung injury and suppressed the cell adhesion molecules in lung tissue. These findings indicate that LTL may prove to be a potential anti-inflammatory agent and provide protection against gram-negative bacterial sepsis with pulmonary impairment.

Show MeSH
Related in: MedlinePlus