Key result
B-type natriuretic peptide acts as an important negative modulator of the neutrophil burst via inhibition of NADPH oxidase, though its effectiveness is partially lost in acute heart failure.
Why the study?
Excessive or prolonged neutrophil activation causes substantial tissue injury in conditions such as heart failure and takotsubo syndrome, prompting discussion of the therapeutic implications of BNP modulation.
BNP modulates neutrophil-initiated myocardial inflammation by inhibiting NADPH oxidase, presenting a potential therapeutic target for acute and chronic cardiac injury.
Activation of neutrophils is a critically important component of the innate immune response to bacterial and chemical stimuli, and culminates in the “neutrophil burst”, which facilitates neutrophil phagocytosis via the release of superoxide anion radical (O2−) from NADPH oxidase. Excessive and/or prolonged neutrophil activation results in substantial tissue injury and increases in vascular permeability—resulting in sustained tissue infiltration with neutrophils and monocytes, and persistent vasomotor dysfunction. Cardiovascular examples of such changes include acute and chronic systolic and diastolic heart failure (“heart failure with preserved ejection fraction”), and the catecholamine-induced inflammatory disorder takotsubo syndrome. We have recently demonstrated that B-type natriuretic peptide (BNP), acting via inhibition of activation of neutrophil NADPH oxidase, is an important negative modulator of the “neutrophil burst”, though its effectiveness in limiting tissue injury is partially lost in acute heart failure. The potential therapeutic implications of these findings, regarding the development of new means of treating both acute and chronic cardiac injury states, are discussed.
No takes yet. Share an insight, caveat, or question.
Liu et al. (2018) conducted a review in Myocardial inflammation and heart failure. B-Type Natriuretic Peptide was evaluated. B-type natriuretic peptide acts as an important negative modulator of the neutrophil burst via inhibition of NADPH oxidase, though its effectiveness is partially lost in acute heart failure.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: