Abstract

The host responses to disease agents differ between age and sex as is evidenced from epidemiological studies which have been ascribed to the effects of steroid hormones. The present study was carried out in 20 Murrah buffaloes of either sex at pre- and post-pubertal age having discrete sex steroid background to explore the variation, if any, in physiological and immune responses upon intravenous endotoxin challenge (E. coli 055:B5 @ 0.6µg/kg body weight). The rectal temperature, heart rate and respiration rate differed significantly from base values at only 1 h post challenge and reached peak at 4 h. The magnitude of responses determined as area under concentration × time curve (AUC) for these parameters was significantly low in post-pubertal animals of either sex. Plasma tumour necrosis factor alpha (TNFα, a pro-inflammatory cytokine) registered peak at 1 h post challenge which returned to base level value by 8 h post challenge. Responses determined as AUC of TNFα were significantly higher in post-pubertal males. Plasma NOx (an estimate of nitric oxide production) and XO (mediator of superoxide production) significantly differed from base value at 4 h and peaked at 8 h post challenge. Integrated AUC response of NOx was significantly higher in pre-pubertal males and that of XO in pre-pubertal males as well as females. Plasma cortisol (an anti-inflammatory hormone) was significantly different from base value at 2 h and peaked between 4 h and 8 h post challenge; its integrated AUC response was significantly greater in post-pubertal females. Endotoxin challenge resulted into neutrophilia (a stress marker), and the initial hyperglycemia was followed by hypoglycemia in all experimental animals irrespective of age and sex. Pre-pubertal buffaloes had no dominance of gonadal sex steroids in plasma. Post-pubertal males and females had plasma testosterone and oestrogen, respectively in significant quantity. The present findings in Murrah buffaloes recognise the age and sex as a source of variability in the magnitude of immune responses to endotoxin challenge like lipopolysaccharide (LPS).

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