Along with B and T cell hyperplasia we found that serum from PD-1 /– PD-1 /ontained antibodies specific for comiceents of contained bantibodieslearly indicating a breach in the normal mucospecificemic compartmentalization. Administration oforroad-specomponentsbioficommensal normalization of the activation phenotype of PD-1–/– mice.
This loss of alveolar and systemic cytokine compartmentalization can lead to peripheral organ dysfunction, a condition of difficult clinical management.
However, as a consequence of regional blood flow redistribution and metabolic compartmentalization, high systemic blood flow may not necessarily guarantee sufficient oxygen delivery to all tissues [ 13, 14].
The compartmentalization of systemic and gut mucosal immunity apparatuses focuses adaptive immunity on gut microbes specifically at the level of the bowel.
In the present study, we did not find an association between higher CMD-IL-6 levels and systemic inflammation, supporting the idea of compartmentalization of the central nervous system.
During systemic infection, activation of coagulation facilitates compartmentalization of pathogens in liver microvessels and limits infection expansion.
Animal findings and results of human sepsis are complementary, and they suggest a compartmentalization of lipid peroxidation in systemic infections by MDR gram-negative bacteria.
The complementary findings between the described animal model and human sepsis are highly indicative of an existing compartmentalization of lipid peroxidation in systemic infections with MDR gram-negative bacteria.
These findings coming from an experimental infection model that are confirmed from a patient cohort clearly indicate that, during systemic infections, lipid peroxidation is characterized by high compartmentalization.
Once compartmentalization of alveolar TNF- α is lost, injured lung may contribute to a systemic inflammatory response and subsequent multiorgan failure [ 60].
Finally, the usual compartmentalization of an infection such as ventriculitis makes it unable to trigger a systemic inflammatory response expressed by serum biomarkers such as C-reactive protein or procalcitonin.
