Influenza and other respiratory viral infections account
for 80%-90% of infectious pathologies. Influenza A (H5N1) virus has an apparent
pneumotropism, and therefore the lung compartment of mononuclear phagocyte
system plays an important role in antiviral immunity. Lung macrophages are
active phagocytes expressing variety of antiviral factors. The investigation of
morphofunctional status of lung macrophages and evaluation of their role in
mammal antiviral response in a mouse model were performed within the study. Methods:
Light microscopy using standard hematoxylin-eosin, and Van-Gizon’s picrofuchsin
staining. Immunohistochemistry using influenza A antigen marker specific
primary antibodies, myeloperoxidase, cathepsin D, lysozyme, NO synthase, pro-inflammatory
cytokines, cells of CD68 macrophage lineage, PCNA proliferative activity.
Morphometric and statistical analysis. Results: Influenza A virus antigen was
detected in lung macrophages starting from day 1 to day 14 of infection which
corresponds with the beginning of convalescence and may be suggestive of
prolonged persistence of virus. On the one hand, the cytopathic effects of the
virus lead to lung macrophages death mainly via apoptosis through activation of
caspase cascade, including caspase-3 and caspase-9. On the other hand, the
observed activation of PCNA proliferation marker, perhaps, allows to support
the pool of lung macrophages not only by their recruitment from bone marrow but
also by their proliferation in situ.
The increase of mononuclear phagocyte system cells expressing antiviral factors
depended on the stage of infection. In the early stage, there was an increase
of number of cells expressing lysozyme, myeloperoxidase, cathepsin D,
endothelial NO synthase (eNOS) followed by the increase of number of macrophages expressing inducible NO synthase
(iNOS), pro-inflammatory cytokines and interleukins.