Studies on effect of gadolinium chloride in Pasteurella multocida inducedlung injury in buffalo calves

ASIYA  MUSHTAQ; A K  ARORA; R S  SETHI; C S  RANDHAWA

doi:10.56093/ijans.v95i1.146364

Authors

ASIYA MUSHTAQ V S Molecular Diagnostics Pvt. Ltd., New Delhi
A K ARORA CoVS, Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana, Punjab
R S SETHI Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana, Punjab 141 012
C S RANDHAWA Guru Angad Dev Veterinary and Animal Sciences University, Ludhiana, Punjab 141 012

https://doi.org/10.56093/ijans.v95i1.146364

Keywords:

Cytokine gene expression, Gadolinium chloride, IL-1β, IL-8, IL-10, Pulmonary intravascular macrophages (PIMs), P. multocida, Real Time PCR, TNF-α

Abstract

Haemorrhagic septicemia (HS) is a fatal disease of cattle and buffaloes caused by Pasteurella multocida (P. multocida) characterized by an early stage of high fever, respiratory involvement followed by septicemia and recumbency resulting in death. Lung inflammation caused by P. multocida results in the expression of cytokines, chemokines and employment of neutrophils and pulmonary intravascular macrophages (PIMs). PIMs secrete various pro-inflammatory cytokines like Tumor-necrosis factor- α (TNF-α), interleukin-8 (IL-8) and IL-6, contributing to acute lung inflammation and lung damage caused by P. multocida. In our study, we aimed to deplete PIMs by use of drug Gadolinium chloride to study the molecular mechanisms of cytokine expression in P. mutocida challenged animals. The expression of genes encoding the cytokines TNF-α, IL-1β, IL-8 and IL-10 in buffalo lung tissues was studied using Real time PCR. Buffalo calves were divided into four treatment groups, viz. Group I (control), Group II (GC treated), Group III (P. multocida challenged) and Group IV (GC pre-treated followed by P. multocida challenge). The upregulation of pro-inflammatory cytokines (TNF- α, IL-1β and IL-8) in Group III indicated their role in promoting lung injury. The down regulation of pro-inflammatory cytokine expressions in Group IV revealed inhibition of PIMs. Depletion of PIMS plays a major role in pathogenesis of HS and may be targeted as a future therapeutic strategy to reduce lung damage associated with P. multocida infections.

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