PMID- 10392755
OWN - NLM
STAT- MEDLINE
DCOM- 19990830
LR  - 20190921
IS  - 0360-3997 (Print)
IS  - 0360-3997 (Linking)
VI  - 23
IP  - 3
DP  - 1999 Jun
TI  - Loxosceles spider venom induces the production of alpha and beta chemokines: 
      implications for the pathogenesis of dermonecrotic arachnidism.
PG  - 207-15
AB  - 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 alpha 
      and beta chemokine families. Because arachnid envenomation results in the 
      exposure of several different cell types to venom, we investigated venom-induced 
      expression of alpha and beta 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 alpha chemokines: interleukin-8 (IL-8), 
      growth-related oncogene-alpha (GRO-alpha), and beta 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 Laxosceles venom resulted in 
      the production of IL-8 (5.2+/-1.30 ng/ml), MCP-1 (1.44+/-0.11 ng/ml) and 
      GRO-alpha (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-alpha 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 alpha and beta chemokines in both endothelial and epithelial cell 
      types. Based on the established roles of IL-8, MCP-1, and GRO-alpha, in 
      inflammation, these observations have relevance to the pathophysiology of 
      Loxosceles-induced dermonecrosis.
FAU - Gomez, H F
AU  - Gomez HF
AD  - Department of Surgery, University of Michigan Medical Center, USA.
FAU - Miller, M J
AU  - Miller MJ
FAU - Desai, A
AU  - Desai A
FAU - Warren, J S
AU  - Warren JS
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Inflammation
JT  - Inflammation
JID - 7600105
RN  - 0 (Chemokines, CC)
RN  - 0 (Chemokines, CXC)
RN  - 0 (Dermotoxins)
RN  - 0 (Spider Venoms)
RN  - 0 (loxosceles venom)
RN  - EC 3.1.4.- (Phosphoric Diester Hydrolases)
SB  - IM
MH  - Cells, Cultured
MH  - Chemokines, CC/*biosynthesis
MH  - Chemokines, CXC/*biosynthesis
MH  - Dermotoxins/*pharmacology
MH  - Endothelium, Vascular
MH  - Epithelial Cells
MH  - Humans
MH  - Lung
MH  - Necrosis
MH  - Phosphoric Diester Hydrolases/*pharmacology
MH  - Skin Diseases/*etiology/pathology
MH  - Spider Bites/*etiology
MH  - Spider Venoms/*pharmacology
MH  - Umbilical Veins
EDAT- 1999/07/07 00:00
MHDA- 1999/07/07 00:01
CRDT- 1999/07/07 00:00
PHST- 1999/07/07 00:00 [pubmed]
PHST- 1999/07/07 00:01 [medline]
PHST- 1999/07/07 00:00 [entrez]
AID - 10.1023/a:1020217818245 [doi]
PST - ppublish
SO  - Inflammation. 1999 Jun;23(3):207-15. doi: 10.1023/a:1020217818245.