The impact of subclinical hyperketonemia on primary immunoglobulins, immune-antioxidant enzymes and acute-phase proteins in postparturient Indian mithun (Bos frontalis) cows reared semi-intensively.

Abstract

Managing subclinical ketosis (SCK), which Indian mithun (Bos frontalis) cows experience at least once within four weeks postpartum, requires understanding the interaction of immuno-inflammatory mediators and hyperketonemia. This study aimed to explore the interplay of SCK with the major immunoglobulins (IgG, IgA), acute-phase proteins (haptoglobin, Hpt; serum amyloid A, SAA), and immune-antioxidant enzymes (lactoperoxidase, LPO; lysozyme, LZM; superoxide dismutase, SOD) in postparturient mithun cows. Thirty SCK mithun cows were selected based on blood BHBA (&#x2265;1.10&#x202f;mmol/l) from two semi-intensive mithun farms. Serum concentrations of IgG, IgA, Hpt, SAA, LPO, LZM and SOD were measured at 1, 2 and 4 weeks postpartum by enzyme-linked immunosorbent assay. SCK group had significantly lower IgA values in the first week postpartum and higher IgG values in the second and fourth week. Higher concentrations (P&#x202f;<&#x202f;0.05) of Hpt, SAA, SOD, and LZM were seen in SCK mithuns during the first week postpartum compared to healthy controls. No significant differences were observed in postpartal LPO. Hpt and SAA concentrations showed a significant positive correlation with BHBA (R=0.39, P&#x202f;<&#x202f;0.001 and R=0.27, P&#x202f;<&#x202f;0.001, respectively) and NEFA (R=0.17, P&#x202f;<&#x202f;0.01 and R=0.13, P&#x202f;<&#x202f;0.001, respectively). Serum IgA and SCK biomarkers (BHBA, NEFA) had negative relationships (R=0.44, P&#x202f;<&#x202f;0.001 and R=0.41, P&#x202f;<&#x202f;0.05, respectively). These findings illustrate that immunologic dysregulation, inflammation and oxidative stress mediate less severe ketosis (SCK) in the early postpartum mithun cows. Conclusively, this justifies the need of developing strategies to control postpartum hyperketonemia in mithun cows. Future studies on the viability of using antiinflammatory and antioxidant therapy to prevent SCK from worsening to clinical ketosis are warranted.