Mononuclear Cells In Lung Research Articles

Development of a peptide-generated antibody to rabbit hemorrhagic disease virus 2 VP60 and its immunohistochemical application in natural cases.

Rabbit hemorrhagic disease virus 2 (RHDV2) has spread across the United States infecting and causing death in domestic and wild rabbits. Immunohistochemistry (IHC) would be a useful tool for the detection of RHDV2 antigen in tissues as it is inexpensive and readily achievable in most diagnostic laboratories. However, there is no readily available antibody for this purpose. To fill this void, we generated an RHDV2 capsid protein VP60-specific antibody in chicken eggs and validated the antibody using formalin-fixed tissues from 5 domestic rabbits naturally infected with RHDV2. Viral antigen was detected immunohistochemically in various tissues, most prominently in hepatocytes and macrophages in liver, and in macrophages in spleen and cecal lymphoid tissue. Intravascular mononuclear cells in lung and renal tubular and biliary epithelium also were immunolabeled. Both nuclear and cytoplasmic immunolabeling were observed. This peptide-generated antibody is a potentially useful tool as an adjunct to reverse-transcription PCR or in situ hybridization for detection of RHDV2 in tissues.

CD4+ T cells mediate respiratory syncytial virus (RSV)-induced airway inflammation through secreting Th2 cytokines

Objective To investigate the role of CD4+ T cells in airway inflammation induced by respiratory syncytial virus (RSV) infection. Methods Animal models of acute RSV infection were established. Lung tissues were stained with hematoxylin and eosin (HE) to observe histopathological changes. Total number of CD4+ T cells and the number of CD4+ T cells secreting Th1/Th2 cytokines (IFN-γ, IL-4, IL-5 and IL-13) in spleen were detected by flow cytometry. Adoptive transfer of CD4+ T cells was performed to identify the role of CD4+ T cells in RSV-induced airway inflammation. Results RSV infection increased the total number of splenic CD4+ T cells, particularly Th2-type CD4+ T cells. The absolute numbers of IL-4/IL-5/IL-13-secreting CD4+ T cells were increased significantly after RSV infection. Furthermore, adoptive transfer of CD4+ T cells into BALB/c mice not only promoted the infiltration of mononuclear cells in lung, but also enhanced the secretion of Th2 cytokines during RSV infection. Conclusion CD4+ T cells are involved in RSV-induced airway inflammation through secreting Th2 cytokines. Key words: Respiratory syncytial virus; CD4+ T cell; Airway inflammation

Beta-chemokines are produced in lungs of mice with mycoplasma respiratory disease.

The recruitment of mononuclear cells in lungs is a key event in the pathogenesis of mycoplasma respiratory disease, but the cascade of events responsible is unknown. Studies were conducted to determine whether beta-chemokines, which are chemotactic for lymphocytes and macrophages, are produced in murine mycoplasma respiratory disease. Our results show that mRNA expression of the macrophage chemoattractant factor (MCP-1) and macrophage inflammatory peptides (MIP-1alpha and MIP-1beta), but not RANTES, increases in Mycoplasma pulmonis-infected mice. Also, MCP-1 concentrations were much higher in lung extracts from mycoplasma-infected mice than in uninfected mice. As beta-chemokines are chemotactic for lymphocytes and macrophages, these results suggest that MCP-1, MIP-1alpha, and/or MIP-1beta, but not RANTES, contribute to mononuclear cell infiltration associated with murine mycoplasma respiratory disease. Thus, the activation of cells to produce beta-chemokines is associated with mycoplasma infection, and the beta-chemokines, along with other factors and cytokines, are most likely involved in the cascade of events leading to mycoplasma inflammatory disease.