Chlorhexidine digluconate has been used as a topical antiseptic in the treatment of acne vulgaris and periodontitis. The acute phase of these diseases involves neutrophilic infiltration. Neutrophil activation and recruitment to inflammatory sites are crucial in both protection against bacterial infections and induction of hystotoxic damage.
Activated neutrophils release several enzymes (elastase and myeloperoxidase [MPO]), which contribute to tissue injury through the direct toxic activity, the generation of oxidants and the inactivation of protective factors, such as alpha-1-antitrypsin (alpha-1-AT). In the present study, we investigated if chlorhexidine might modulate neutrophil-mediated histotoxicity.
2. Human primary neutrophils were isolated from healthy donors. Inactivation of alpha-1-AT by neutrophils or reagent hypochlorous acid (HOCl) was evaluated by spectrophotometer and SDS-PAGE analysis of its capacity to complex with porcin pancreatic elastase (PPE). Neutrophil generation of HOCl, superoxide anion and MPO release were assessed spectrophometrically.
3. Chlorhexidine dose-dependently prevented HOCl-induced alpha-1-AT inactivation and reduced HOCl recovery by PMA-treated human neutrophils. Chlorhexidine did not inhibit superoxide anion and MPO release by phorbol-12-myristate-13-acetate (PMA)-treated neutrophils. Chlorhexidine directly inhibited HOCl recovery from neutrophils and HOCl-induced inactivation of alpha-1-AT in a cell-free assay.
Accordingly, chlorhexidine reversed HOCl-mediated inhibition of alpha-1-AT capacity to complex with PPE. 4. These data suggest that chlorhexidine prevents neutrophil-induced alpha-1-AT inactivation through the direct inhibitory activity on HOCl. Although highly speculative, the present article indicates that chlorhexidine might protect inflamed tissues not only through its antimicrobial properties, but also through a direct anti-inflammatory activity on neutrophil toxic products.
"Chlorhexidine prevents hypochlorous acid-induced inactivation of alpha-1-antitrypsin (alpha-1-AT)."
Clin Exp Pharmacol Physiol. 2009 Aug 4; Montecucco F, Bertolotto M, Ottonello L, Pende A, Dapino P, Quercioli A, Mach F, Dallegri F1.(hubmed.org)
Related:
Hypochlorous acid-induced heme oxygenase-1 gene expression
Inhibition of myeloperoxidase-mediated hypochlorous acid
The pro-inflammatory oxidant hypochlorous acid induces
Biochemistry: Homemade Hydrochloride Acid, Sodium Hydroxide
what does hypochlorous acid mean?
Hypochlorous acid
Effectiveness of hypochlorous acid and glutaraldehyde high level
Hypochlorous Acid, Where Have you Been all my Life?
Effects of a Low Concentration Hypochlorous Acid Nasal Irrigation
Oxidation of ovarian epithelial cancer cells by hypochlorous acid
Hypochlorous acid-mediated generation of glycerophosphocholine
Wound Antiseptic Study With Hypochlorous Acid & Iodopovidone
Activated neutrophils release several enzymes (elastase and myeloperoxidase [MPO]), which contribute to tissue injury through the direct toxic activity, the generation of oxidants and the inactivation of protective factors, such as alpha-1-antitrypsin (alpha-1-AT). In the present study, we investigated if chlorhexidine might modulate neutrophil-mediated histotoxicity.
2. Human primary neutrophils were isolated from healthy donors. Inactivation of alpha-1-AT by neutrophils or reagent hypochlorous acid (HOCl) was evaluated by spectrophotometer and SDS-PAGE analysis of its capacity to complex with porcin pancreatic elastase (PPE). Neutrophil generation of HOCl, superoxide anion and MPO release were assessed spectrophometrically.
3. Chlorhexidine dose-dependently prevented HOCl-induced alpha-1-AT inactivation and reduced HOCl recovery by PMA-treated human neutrophils. Chlorhexidine did not inhibit superoxide anion and MPO release by phorbol-12-myristate-13-acetate (PMA)-treated neutrophils. Chlorhexidine directly inhibited HOCl recovery from neutrophils and HOCl-induced inactivation of alpha-1-AT in a cell-free assay.
Accordingly, chlorhexidine reversed HOCl-mediated inhibition of alpha-1-AT capacity to complex with PPE. 4. These data suggest that chlorhexidine prevents neutrophil-induced alpha-1-AT inactivation through the direct inhibitory activity on HOCl. Although highly speculative, the present article indicates that chlorhexidine might protect inflamed tissues not only through its antimicrobial properties, but also through a direct anti-inflammatory activity on neutrophil toxic products.
"Chlorhexidine prevents hypochlorous acid-induced inactivation of alpha-1-antitrypsin (alpha-1-AT)."
Clin Exp Pharmacol Physiol. 2009 Aug 4; Montecucco F, Bertolotto M, Ottonello L, Pende A, Dapino P, Quercioli A, Mach F, Dallegri F1.(hubmed.org)
Related:
Hypochlorous acid-induced heme oxygenase-1 gene expression
Inhibition of myeloperoxidase-mediated hypochlorous acid
The pro-inflammatory oxidant hypochlorous acid induces
Biochemistry: Homemade Hydrochloride Acid, Sodium Hydroxide
what does hypochlorous acid mean?
Hypochlorous acid
Effectiveness of hypochlorous acid and glutaraldehyde high level
Hypochlorous Acid, Where Have you Been all my Life?
Effects of a Low Concentration Hypochlorous Acid Nasal Irrigation
Oxidation of ovarian epithelial cancer cells by hypochlorous acid
Hypochlorous acid-mediated generation of glycerophosphocholine
Wound Antiseptic Study With Hypochlorous Acid & Iodopovidone
