Immunopathogenesis of porcine reproductive and respiratory syndrome in the respiratory tract of pigs

• Published in: The veterinary journal (1997) Vol. 195; no. 2; pp. 148 - 155
• Main Authors: Gómez-Laguna, Jaime, Salguero, Francisco J., Pallarés, Francisco J., Carrasco, Librado
• Format: Journal Article
• Language: English
• Published: England Elsevier Ltd 01.02.2013
• Subjects: Acute phase proteins; Animals; antibacterial properties; apoptosis; bacterial infections; Cytokines; haptoglobins; immune response; interleukin-10; Macrophages; necrosis; neoplasms; Pathogenesis; pathogenicity; porcine reproductive and respiratory syndrome; Porcine Reproductive and Respiratory Syndrome - immunology; Porcine Reproductive and Respiratory Syndrome - pathology; Porcine reproductive and respiratory syndrome virus; Porcine respiratory and reproductive syndrome virus; respiratory system; Respiratory System - cytology; Respiratory System - immunology; Respiratory System - pathology; Swine; tumor necrosis factor-alpha; vaccines; virus receptors; virus replication; viruses; Porcine reproductive and respiratory syndrome virus; Cytokines; Macrophages; Pathogenesis; Acute phase proteins
• ISSN: 1090-0233; 1532-2971
• DOI: 10.1016/j.tvjl.2012.11.012

Porcine reproductive and respiratory syndrome (PRRS) virus (PRRSV) impairs local pulmonary immune responses by damaging the mucociliary transport system, impairing the function of porcine alveolar macrophages andinducing apoptosis of immune cells. An imbalance between pro- and anti-inflammatory cytokines, including tumour necrosis factor-α and interleukin-10, in PRRS may impair the immune response of the lung. Pulmonary macrophage subpopulations have a range of susceptibilities to different PRRSV strains and different capacities to express cytokines. Infection with PRRSV decreases the bactericidal activity of macrophages, which increases susceptibility to secondary bacterial infections. PRRSV infection is associated with an increase in concentrations of haptoglobin, which may interact with the virus receptor (CD163) and induce the synthesis of anti-inflammatory mediators. The balance between pro- and anti-inflammatory cytokines modulates the expression of CD163, which may affect the pathogenicity and replication of the virus in different tissues. With the emergence of highly pathogenic PRRSV, there is a need for more information on the immunopathogenesis of different strains of PRRS, particularly to develop more effective vaccines.