Role Of Sgk-1 In Resistance To Infection Of Salmonella Typhimurium In Caenorhabditis Elegans

The study of the host-bacteria interaction mechanism has far-reaching and extensive implications for ecosystems,agriculture,and human health.Among them,Caenorhabditis elegans is often used as an important model organism to study the host-bacterial interaction mechanism.Similar to other invertebrates,Caenorhabditis elegans does not have an adaptive immune system or specific immune cells,but it can resist infection by pathogens through natural immune mechanisms.Due to its environmental and dietary characteristics,Caenorhabditis elegans is extremely vulnerable to attack by microorganisms,especially microorganisms that inhabit its epidermis and intestinal tract.This paper aims to study the intracellular bacterium Salmonella Typhimurium and the extracellular bacterium Pseudomonas aeruginosa infecting Caenorhabditis elegans,sgk-1(encoding serine/threonine protein kinase)and The role of cyp-23A1(encoding cytochrome P450 homologous to the human gene cyp7B1)in the innate immunity of nematodes.Our study showed that there was no significant change in the survival rate of sgk-1mutant nematodes compared with wild-type nematodes when infected with Pseudomonas aeruginosa;in the case of Salmonella typhimurium infection,sgk-1mutant nematodes and wild-type The survival rate of nematodes increased.It has been reported in the literature that cyp-23A1 can inhibit sgk-1 in Caenorhabditis elegans.However,we found that the survival rate of cyp23A1 mutant nematodes did not change significantly compared with wild-type nematodes when infected with Salmonella typhimurium or Pseudomonas aeruginosa.Therefore,we hypothesize that the increase in survival caused by S.typhimurium-infected sgk-1 mutant nematodes may be achieved through other signaling pathways.It has been reported in the literature that SGK1 negatively regulates phosphorylation of TAK1,a member of the MAPKK kinase family,in mice,whereas TAK1 phosphorylation activates the expression of downstream related inflammatory factors.It is the mom-4 gene that is homologous to TAK1 in Caenorhabditis elegans.Our study found that when Salmonella typhimurium infects Caenorhabditis elegans,the survival rate of mom-4 nematodes is significantly reduced.When the same Salmonella typhimurium infection occurred,the survival rate of the nematode recovered to wild-type nematode level after disturbing mom-4 in the sgk-1mutant nematode.In typhoid salmonella infestation,sgk-1 mutation resulted in increased expression of mom-4.The above results indicate that sgk-1 negatively regulates the natural immune response of nematodes by inhibiting mom-4 when infected with Salmonella typhimurium.In summary,our study revealed that sgk-1 is not involved in C.elegans immunity when infected with Pseudomonas aeruginosa,but sgk-1 inhibits mom-4 by typhoid Salmonella infestation.Negatively regulates the natural immune response of Caenorhabditis elegans.