Inflammation

, Volume 23, Issue 3, pp 207–215

Loxosceles Spider Venom Induces the Production of α and β Chemokines: Implications for the Pathogenesis of Dermonecrotic Arachnidism

  • Hernan F. Gomez
  • Mark J. Miller
  • Anjali Desai
  • Jeffrey S. Warren

Abstract

Bites from the brown recluse spider and other Loxosceles arachnids result in dermonecrotic skin lesions. Neutrophils (PMN) are essential to the development of Loxosceles-induced skin lesions, but paradoxically, in vitro PMN activation is inhibited by direct exposure to Loxosceles venom. Neutrophil activation occurs in response to a myriad of soluble mediators that include members of both the α and β chemokine families. Because arachnid envenomation results in the exposure of several different cell types to venom, we investigated venom-induced expression of α and β chemokines in both endothelial cells (human umbilical vein; HUVEC) and epithelial cells (A549 pneumocytes). Chemokine-specific capture enzyme immunoassays (EIA) were used to measure Loxosceles deserta venom-induced α chemokines: interleukin-8 (IL-8), growth-related oncogene-alpha (GRO-α), and β chemokines: monocyte chemoattractant protein-1 (MCP-1), and regulated on activation, normal T cell expressed and secreted (RANTES) in cell-free conditioned media from HUVEC and A549 cell monolayers. Exposure of HUVECs (8 h) to Loxosceles venom resulted in the production of IL-8 (5.2 ± 1.30 ng/ml), MCP-1 (1.44 ± 0.11 ng/ml) and GRO-α (1.97 ± 0.15 ng/ml) in a dose and time-dependent manner. Exposure of A549 cell monolayers to venom resulted in IL-8 (7.74 ± 0.30 ng/ml), and MCP-1 (2.61 ± 0.31 ng/ml), but neither GRO-α nor RANTES accumulated during an 8-hour incubation period. Chemokines accumulated in a venom dose and time-dependent manner. Neither cell type secreted RANTES in response to Loxosceles venom. These data indicate that Loxosceles spider venom is a potent inducer of α and β chemokines in both endothelial and epithelial cell types. Based on the established roles of IL-8, MCP-1, and GRO-α, in inflammation, these observations have relevance to the pathophysiology of Loxosceles-Induced dermonecrosis.

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Copyright information

© Plenum Publishing Corporation 1999

Authors and Affiliations

  • Hernan F. Gomez
    • 1
  • Mark J. Miller
    • 2
  • Anjali Desai
    • 2
  • Jeffrey S. Warren
    • 2
  1. 1.Department of SurgerySection of Emergency MedicineUSA
  2. 2.Department of PathologyUniversity of Michigan Medical CenterUSA

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