NETosis and lack of DNase activity are key factors in Echis carinatus venom-induced tissue destruction

Gajanan D. Katkar, Mahalingam S. Sundaram, Somanathapura K. NaveenKumar, Basavarajaiah Swethakumar, Rachana D. Sharma, Manoj Paul, Gopalapura J. Vishalakshi, Sannaningaiah Devaraja, Kesturu S. Girish () and Kempaiah Kemparaju ()
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Gajanan D. Katkar: University of Mysore, Manasagangothri
Mahalingam S. Sundaram: University of Mysore, Manasagangothri
Somanathapura K. NaveenKumar: University of Mysore, Manasagangothri
Basavarajaiah Swethakumar: University of Mysore, Manasagangothri
Rachana D. Sharma: University of Mysore, Manasagangothri
Manoj Paul: University of Mysore, Manasagangothri
Gopalapura J. Vishalakshi: University of Mysore, Manasagangothri
Sannaningaiah Devaraja: Tumkur University
Kesturu S. Girish: University of Mysore, Manasagangothri
Kempaiah Kemparaju: University of Mysore, Manasagangothri

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract Indian Echis carinatus bite causes sustained tissue destruction at the bite site. Neutrophils, the major leukocytes in the early defence process, accumulate at the bite site. Here we show that E. carinatus venom induces neutrophil extracellular trap (NET) formation. The NETs block the blood vessels and entrap the venom toxins at the injection site, promoting tissue destruction. The stability of NETs is attributed to the lack of NETs-degrading DNase activity in E. carinatus venom. In a mouse tail model, mice co-injected with venom and DNase 1, and neutropenic mice injected with the venom, do not develop NETs, venom accumulation and tissue destruction at the injected site. Strikingly, venom-induced mice tail tissue destruction is also prevented by the subsequent injection of DNase 1. Thus, our study suggests that DNase 1 treatment may have a therapeutic potential for preventing the tissue destruction caused by snake venom.

Date: 2016
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DOI: 10.1038/ncomms11361

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