Is the induction of NETs or NETosis often result to the death of neutrophil? are the mechanisms for neutrophil or host defense?
Curious to know wheither the processes are just to mediate pathogen killing or itself will go for it. I read that the processes were for protection of neutrophil against invasion cytosolic pathogen. confuse!!!
There are two forms of NETs formation in neutrophil, SUICIDE and Non-suicide or vital NETs formation, in suicidal NETs formation, neutrophils rupture their plasma membrane to release extracellular DNA, histones and elastase and chromatin fibers and as such they are killed in the process and this is mostly seen when you activate them with PMA in vitro, however the non-suicidal NETs formation, neutrophils release NETs via blebbing of the nuclear envelope and vesicular exportation without compromising the integrity of the plasma membrane and it mostly occur when you activate neutrophils with LPS. The behavior of neutrophil in terms of NETs formation also depends on the type of pathogen(especially among bacteria).
Thanks Kehinde Adebayo Babatunde but are the protective capacities of the two type are same cum their harmful effects. however, do aware now that there is noncanonical pathways that bypassed the classical procedure of NETs activation. I am just wondering with NETosis-induced gasdermin cleavage, can Neutrophil release its cytosolic resident pathogen and also mediate extracellular protection ?
Abdulkareem Olarewaju Babamale NETs formation in neutrophils is a tricky process And the exact pathway is still confusing. its formation is triggered by pathogens to immobilize them and kill them so therefore its part of the neutrophil host defense mechanism. However, there are disease states where NETs formation have been implicated to cause serious inflammatory conditions( lupus and Lyme patients). Over production of NETs during sepsis has also been linked to multiple organ failures. During malaria, NETs has also been reported to cause clogging of the micro vessels thereby causing anemia( hypothesis tho) etc. So NETs could infact act as both anti inflammatory and pro inflammatory processes. gasdermin cleavage is linked to LPS induced intercellular NETs. it cleaves with caspase 11 to elicit non suicidal NETs. It’s also independent of the known NETs molecule like MPO and PAD4. Via this pathway trapped cytotoxic bacteria are neutralized before they are released from the host neutrophils! I suggest you read Kaiwen Chen paper in science immunology on gasdermin and NETs
Thanks for your submission and I quite agreed with you. I have read those papers you mentioned and others that revealed induction of Netosis via canonical and non-canonical pathways also the conventional pathway induced by ROS with the aid of those molecules you mentioned (MPO, NE & PAD4). Thanks
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