Influence of immunization on the pulmonary inflammatory response of rabbits induced by Pasteurella haemolytica A1 lipopolysaccharide

Abstract

Immune complex formation has long been thought to play a role in the pathogenesis of Pasteurella haemolytica pneumonia. This study in laboratory rabbits was designed to investigate immune-mediated damage in respiratory tissue caused by lipopolysaccharide (LPS). Severe lesions were induced by the intratracheal (IT) injection of P. haemolytica A1 LPS (50 micrograms) into rabbits previously immunized with P. haemolytica killed whole cells emulsified with Freund's incomplete adjuvant (FIA); these lesions included perivascular oedema and polymorphonuclear leucocyte (PMN) infiltration of the subintima, with degeneration and necrosis of the media. Smaller vessels were occluded by PMNs in various stages of degranulation. PMN counts in bronchoalveolar lavage (BAL) fluid were significantly elevated (P < 0.05). Lesions were also induced by the IT injection of LPS (50 micrograms) into rabbits pretreated with an emulsion consisting merely of FIA and formol-saline; these lesions included moderate to severe congestion, interstitial oedema, alveolar serofibrinous exudation and PMN infiltration. PMNs were also present in BAL fluid. Rabbits pretreated with FIA in formol-saline and given a later IT injection of saline, and rabbits pretreated with bovine serum albumin (BSA) in FIA and given a later IT injection of BSA, were included as negative and positive control groups. Cutaneous lesions were also induced by the intradermal injection of LPS into rabbits immunized against P. haemolytica and of BSA into rabbits immunized with BSA. Overall, the pulmonary and cutaneous lesions induced in vaccinated rabbits by antigen administration were more severe than those seen in non-vaccinated rabbits. The lesions in rabbits, which were similar to those seen in natural cases of P. haemolytica pneumonia in cattle, were characterized by a fibrinopurulent inflammatory process with extensive interstitial oedema, fibrinous exudate, and PMNs. This model may help to elucidate the pathogenesis of pneumonic pasteurellosis in immunized animals.