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The models using ex vivo or in vitro experiments with plasma from septic patients or animals have confirmed the presence of molecules in plasma that may alter cellular functions, even for healthy cells.
Immunoglobulins targeting bacterial cytolysins may alter cellular survival as well [25].
It is well known that viruses may alter cellular signaling pathways, in particular PI3-kinase, to control their endocytic movement [35].
The accumulation of lipofuscin may alter cellular autophagic activity.
This suggests that DHA loading may alter cellular redox status.
Calcium levels are lower than in control children, which may alter cellular signaling [ 10].
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In addition to redox reactivity, heme may adversely alter cellular functions by binding to essential proteins and impairing their function.
E2 may partly alter cellular proteome through alternative splicing uncoupled to its effects on transcription initiation and aberration in E2-induced alternative splicing events may influence response to anti-estrogens.
Alterations in the protein level of metabolic enzymes, adaptor proteins and heat shock proteins upon LASP-1 knock down may alter the cellular dynamics or motility.
Moreover, thiol-reactive compounds may alter the cellular redox state and have an impact on the oxidative modifications of proteins [21], [36].
The immediate, transient nature of these signalling events suggests that HSV-1 glycoproteins, particularly gD, may alter the cellular environment pre-entry so as to condition the cell for viral replication.
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