Immuno-reactivity evaluation of Mce-truncated subunit candidate vaccine against Mycobacterium avium subspecies paratuberculosis challenge in the goat models

Abstract

Background Detection of an appropriate antigen with high immunogenicity can be a big step in the production of an effective vaccine for control of Johne’s disease (JD). The aim of this study was to evaluate the efficacy of Mce-truncated protein as a subunit vaccine candidate for the control of JD in experimentally challenged goats. Materials and methods Six healthy goat kids were immunized with Mce-truncated protein, and two goats were kept as controls. All kids were twice challenged orally with live Mycobacterium avium subspecies paratuberculosis(MAP) strain and half the goats from both the categories were sacrificed at 7 and 10 months after start of challenge study. Culture of MAP was performed from all the necropsied tissues to determine the true JD infection status. Results Mce-truncated protein only reacted with pooled vaccinated goat sera in western-blot. A significant increase in humoral immune response against Mce protein was also observed in vaccinated goats. Compared to the control group, vaccinated goats gained higher body weights and none of them shed MAP or showed histopatological lesions or colonization of MAP in their necropsy tissues. Conclusions The new Mce protein based vaccine provided significant immunity in goats as they could meet the challenge with live MAP bacilli. Although the vaccine used in this study showed the high potential as a new effective vaccine for the control of JD, further validation study is still required to successfully implement the vaccine for JD control program.

The role of Mce proteins in Mycobacterium avium paratuberculosis infection

“…From such experiments, FAPs were shown to be upregulated in response to acidic treatment 20 . Although expression of the mce5 cluster of Mce proteins has been seen to elicit an immune response from infected animals 24 and be a possible vaccine candidate in goats 25 , and mutations in mce1D have been shown to reduce the capacity of MAP to infect MDBK cells 18 , whether the expression of these proteins subsequently aids the attachment and invasion of MAP into intestinal epithelial cells remains to be determined 7 .…”