IMMUNE SUPPRESSION BEING THE CAUSE FOR ESTABLISHMENT OF NOSEMA BOMBYCIS PARASITISM IN THE SILKWORM BOMBYX MORI
Pebrine is a devastating disease caused by obligate intracellular microsporidian parasite Nosema bombycis in the silkworm Bombyx mori. Though organismal observations after infection are reported, larval immune responses are seldom analysed. The infection reduced hemocyte number and induced subcellular variations like membrane porosity, lysis and disintegration. On infection, hemocytes recognize pathogens through recognition proteins that trigger defense reactions. However after N. bombycis infection, expression of immune genes pertaining to recognition, Toll signalling and melanization pathways were suppressed, revealed by RT-PCR and Real Time analysis. Recognition genes β-GRP 2 and β-GRP 4 were inactivated thereby delayed or inhibited recognition. Toll activator Spatzle expression was suppressed and titer reduced early causing delayed binding with ‘Toll’. Gene encoding Cactus expression increased whereas expression of NF kappa B transcription factors Dorsal and Relish reduced in early stage of infection. Immediately after infection melanisation pathway genes PPAE and PPO2 activated, subsequently suppressed expression causing loss of ‘melanization’ in later stage of infection. Paralytic peptide titer that induced melaniztion, reduced in early stage of infection. Delayed recognition and signalling activities allowed distraction of N. bombycis from primary immune reactions of the host leading to successful establishment of parasitic survival. Further due to lack of melanisation in later stages, N. bombycis surmount the host – defenses and establish itself in infected larvae of B. mori. Different immune pathway components suppressed by the microsporidian infection could be used as targets for antibody – based early detection mechanisms.
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