Bothrops lanceolatus (Fer de lance) venom stimulates leukocyte migration into the peritoneal cavity of mice

Arruda, Vanessa Alves; Guimarães, Alessandra de Queiroz; Hyslop, Stephen; Araujo, Paulo Maria Ferreira de; Bon, Cassian; Araújo, Albetiza Lôbo de

doi:10.1016/s0041-0101(02)00238-6

Cited by 31 publications

(19 citation statements)

References 44 publications

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“…Incubation of the venom at different temperatures indicated that the venom component responsible for hemolysis is thermolabile. Other biological activities of B. lanceolatus, such as rat paw edema, leukocyte migration and hemorrhagic activity, are also thermolabile (7,21,22 (16,(28)(29)(30)(31)(32).…”

Section: Discussionmentioning

confidence: 99%

In vitro hemolytic activity of Bothrops lanceolatus (fer-de-lance) venom

Martins¹,

Araújo²,

Bon³

et al. 2009

J. Venom. Anim. Toxins incl. Trop. Dis

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Bothrops lanceolatus venom contains a variety of enzymatic and biological activities. The present work investigated the hemolytic activity of this venom and its phospholipase A 2 (PLA 2 ). Bothrops lanceolatus venom (6.7 µg/mL) caused indirect hemolysis of cow, horse, rat and sheep erythrocytes, with horse erythrocytes being the most sensitive; no direct hemolysis was observed. Hemolysis in sheep erythrocytes was concentration-dependent (5-11.7 µg/mL) and markedly attenuated by heating the venom for 30 minutes at ≥ 40°C and by the PLA 2 inhibitor p-bromophenacyl bromide. An acidic PLA 2 (5 µg/mL) purified from B. lanceolatus venom also caused hemolysis. This PLA 2 showed immunoprecipitin lines with antivenom against B. lanceolatus, which suggests that the enzymatic and hemolytic activities of this enzyme may be neutralized during antivenom therapy. These results indicate that B. lanceolatus venom and its PLA 2 can cause hemolysis in vitro.

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Section: Discussionmentioning

confidence: 99%

In vitro hemolytic activity of Bothrops lanceolatus (fer-de-lance) venom

Martins¹,

Araújo²,

Bon³

et al. 2009

J. Venom. Anim. Toxins incl. Trop. Dis

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“…; Arruda et al . ) with over 95% of CD11b‐positive cell percentage, were treated with 10 μg/mL lipopolysaccharide (LPS; L4391 from Sigma‐Aldrich, St. Louis, MO, USA) and 10 ng/mL interleukin‐4 (IL‐4; I1020, Sigma‐Aldrich) in 10% normal horse serum (HS) in Dulbecco's modified Eagle's medium (DMEM low glucose type; 31600‐034 from Invitrogen) for 24 h in order to activate macrophages into M1 and M2 phenotypes, respectively (Gea‐Sorlí & Closa ; Leidi et al . ; Michelucci et al .…”

Section: Methodsmentioning

confidence: 99%

“…Resident macrophages, which were harvested from the abdominal cavity of normal mice by peritoneal washes with ice-cold PBS according to a regular protocol described previously (Souza et al 1988;Arruda et al 2003) with over 95% of CD11b-positive cell percentage, were treated with 10 μg/mL lipopolysaccharide (LPS; L4391 from Sigma-Aldrich, St. Louis, MO, USA) and 10 ng/mL interleukin-4 (IL-4; I1020, Sigma-Aldrich) in 10% normal horse serum (HS) in Dulbecco's modified Eagle's medium (DMEM low glucose type; 31600-034 from Invitrogen) for 24 h in order to activate macrophages into M1 and M2 phenotypes, respectively (Gea-Sorlí & Closa 2009;Leidi et al 2009;Michelucci et al 2009). Cultures with less than 80% CD197-or CD206postive cells were not used for the subsequent experiments, in which mRNA expression of HGF (accession no.…”

Section: Activated Macrophage Culturesmentioning

confidence: 99%

Preliminary time‐course study of antiinflammatory macrophage infiltration in crush‐injured skeletal muscle

Shono

Sakaguchi

Suzuki

et al. 2013

Animal Science Journal

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Muscle damage induces massive macrophage infiltration of the injury site, in which activated pro-inflammatory and anti-inflammatory phenotypes (currently classified as M1 and M2, respectively) have been documented as distinct functional populations predominant at different times after the conventional acute injury by intramuscular injection of snake venoms (cardiotoxin, notexin) or chemicals (bupivacaine hydrochloride, barium chloride). The present study employed a muscle-crush injury model that may better reflect the physiologic damage and repair processes initiated by contusing a gastrocnemius muscle in the lower hind-limb of adult mice with hemostat forceps, and examined the time-course invasion of M1 and M2 macrophages during muscle regeneration by immunocytochemistry of CD197 and CD206 marker proteins. CD197-positive M1 macrophages were observed exclusively at 1-4 days after crush followed by the alternative prevalence of CD206-positive M2 at 7 days of myogenic differentiation, characterized by increasing levels of myogenin messenger RNA expression. Preliminary PCR analysis showed that M2 may produce hepatocyte growth factor (HGF) in culture, providing additional benefit to understanding that M2 populations actively promote regenerative myogenesis (muscle fiber repair) and moto-neuritogenesis (re-attachment of motoneuron terminals onto damaged fibers) through their time-specific infiltration and release of growth factor at the injury site early in muscle regeneration.

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“…To exclude the possibility that the lectin-induced augmentation of the serum level of NO was due to contamination of the lectin preparations with endotoxin, the protocol described by Arruda et al [18] was performed. Lectin (2.0 mg/ml) was incubated (30 min, 37°C) with polymyxin B sulphate (100 mg/ml).…”

Section: Measurement Of Serum No Concentrationmentioning

confidence: 99%