Abstract
Resistance to respiratory disease in cattle requires host defense mechanisms that protect against pathogens which have evolved sophisticated strategies to evade them, including an altered function of pulmonary macrophages (MΦs) or the induction of inflammatory responses that cause lung injury and sepsis. The aim of this study was to clarify the mechanisms responsible for vascular changes occurring in the lungs of calves infected with bovine viral diarrhea virus (BVDV) and challenged later with bovine herpesvirus type 1 (BHV-1), evaluating the role of MΦs in the development of pathological lesions in this organ. For this purpose, pulmonary lesions were compared between co-infected calves and healthy animals inoculated only with BHV-1 through immunohistochemical (MAC387, TNFα, IL-1α, iNOS, COX-2 and Factor-VIII) and ultrastructural studies. Both groups of calves presented important vascular alterations produced by fibrin microthrombi and platelet aggregations within the blood vessels. These findings were earlier and more severe in the co-infected group, indicating that the concomitance of BVDV and BHV-1 in the lungs disrupts the pulmonary homeostasis by facilitating the establishment of an inflammatory and procoagulant environment modulated by inflammatory mediators released by pulmonary MΦs. In this regard, the co-infected calves, in spite of presenting a greater number of IMΦs than single-infected group, show a significant decrease in iNOS expression coinciding with the presence of more coagulation lesions. Moreover, animals pre-inoculated with BVDV displayed an alteration in the response of pro-inflammatory cytokines (TNFα and IL-1), which play a key role in activating the immune response, as well as in the local cell-mediated response.
Highlights
The bovine respiratory disease complex (BRDC) is an important problem for the cattle industry, often resulting in severe economic losses [1,2]
The calves pre-infected with bovine viral diarrhea virus (BVDV) show more intense respiratory signs such as cough, mucopurulent nasal discharge, dyspnoea and open-mouth breathing mainly between 4 and 11 dpi, while the calves of the bovine herpesvirus type 1 (BHV-1) group only presented a moderate serous nasal discharge
Detection of BVDV and BHV-1 in the lungs The presence of BVDV in the lungs of co-infected calves was detected by RT-Polymerase chain reaction (PCR) between 0 and 7 dpi (12–19 dpi BVDV), presenting the samples cycle threshold values between 33 and 39; whereas BHV-1 was detected by PCR from 2 to 14 dpi in these calves with cycle threshold values from 35 to 40
Summary
The bovine respiratory disease complex (BRDC) is an important problem for the cattle industry, often resulting in severe economic losses [1,2] This fatal bovine respiratory infection is a multi-factorial disease associated with a primary viral infection followed by a secondary bacterial infection. Increased blood supply, enhanced vascular permeability and migration of immune cells occur at damaged sites. In this process, MΦs play a central role in managing different immunopathological phenomena through the secretion of inflammatory mediators such as nitric oxide (NO), prostaglandins, and the pro-inflammatory cytokines tumor necrosis factor-α (TNFα) and interleukin (IL)-1 [9,10,11]
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