Overstimulation of leukocytes, cytokine storm, and altered tissue repair are key contributors to ARDS severity, mortality, and long-term morbidity [3].
Therefore, decreased leukocyte activation in infected CCR2 /– mice may explain the decreased cytokine storm and decreased tissue damage observed in these animals.
They use the host's gut cytokine storm and the associated tissue injury to promote their tissue invasion.
Factors implicated in the high morbidity and mortality associated with influenza virus infection include, but are not limited to, a robust cytokine production (cytokine storm), excessive inflammatory infiltrates, virusnduced tissue destruction [ 6], and secondary bacterial coinfection [ 7].
They are characterized by so-called systemic cytokine storms, cell damage and death, tissue injury, and may ultimately result in multiple organ dysfunction syndrome (MODS) and death if not curbed in time.
This route of administration was chosen because the skin contains DCs previously demonstrated to actively promote CTL activity (Campton et al, 2000), and because after application liposomes distribute preferentially via the lymph reaching local organised lymphoid tissues (Oussoren and Storm, 2001).
An overly strong immune response with a cytokine storm [ 2], mitochondriopathy, and massive tissue damage may lead to early death [ 3].
Cytokine storms can result in autoimmune reactions, tissue damage, or septic shock.
Factors implicated in influenza-mediated morbidity and mortality include robust cytokine production (cytokine storm), excessive inflammatory infiltrates, and virus-induced tissue destruction.
The infectious pathogen and damaged host tissue create a cytokine and chemokine "storm" in the early phase of sepsis that activates the innate and adaptive host responses.
