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Clarke et al. (2010), have demonstrated peptidoglycan from the commensal microbiota modulate the innate immune system by improving neutrophil function even in the absence of infection.
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It may therefore provide a therapeutic option to improve neutrophil function during septic hyperresistinemia and ultimately alleviate immunosuppression in this disease state.
Adjuvant hyperbaric oxygen therapy improves neutrophil function, fibroblast proliferation and collagen secretion, each of which is important in infection control and wound coverage.
In vitro treatment with interferon-γ and granulocyte-macrophage colony-stimulating factor has improved neutrophil function agranulocyte-macrophage colony-stimulating
Maitake beta-glucan consumption improves neutrophil and monocyte function in lower-risk MDS patients.
As deregulated excessive C5a activity is likely to be a key molecular mechanism in sepsis [ 7, 106], C5a scavenging by IVIg therapy should improve neutrophil [ 27] and myocardial function [ 101], as well as reducing coagulopathy [ 102], immune cell apoptosis [ 28, 107- 109] and autonomic nervous system dysfunction.
In addition, trace element supplementation is likely to improve neutrophil, macrophage, and lymphocyte function in severely burned patients; in truth, we observed higher neutrophil counts in the supplemented patients of the first trial [ 15].
As these represent downstream mediators scavenged by IVIg, IVIg therapy could restore neutrophil function and improve bacterial clearance.
Sepsis is marked by significant changes in neutrophil function, including the induction of endothelial barrier dysfunction.
Intriguingly, these protective effects were mediated by a mechanism independent of neutrophil function.
Modulation of this key neutrophil function by endogenous agents and the mechanisms involved are poorly understood.
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