title: Human milk anti-inflammatory component contents during acute mastitis.
abstract: Mastitis is a common complication of human lactation. We examined milk specimens from eight women with clinical mastitis to determine their content of anti-inflammatory components. Antioxidant activity (spontaneous cytochrome c reducing activity), selected pro-inflammatory cytokines (IL-6, IL-1beta), selected endogenous cytokine control molecules (sIL-6R, sIL-1RII, and sTNFRI), lactoferrin, Na(+):K(+) ratios, and milk bioactivities that cause shedding of sIL-1RII from human polymorphonuclear leukocytes (PMN), suppress PMN aggregation, and suppress PMN adherence responses were not increased compared to normal milks. Neither the bioactivities that deplete PMN intracellular Ca(2+) stores nor those that block Ca(2+) influx into fMLP-stimulated PMN were significantly increased in mastitis milks. In contrast, levels of TNFalpha, sTNFRII, and IL-1RA and bioactivities that cause shedding of sTNFRI from human PMN were significantly increased compared to normal milks. Mastitis milk has the same anti-inflammatory components and characteristics of normal milk, with elevations in selected components/activities that may help protect the nursing infant from developing clinical illness due to feeding on mastitis milk.
authors.affiliation: Center for Pediatric Research, Children's Hospital of The King's Daughters, Norfolk, Virginia 23510, USA.
authors.forename: E S
authors.initials: ES
authors.lastname: Buescher
authors.forename: P S
authors.initials: PS
authors.lastname: Hair
mesh_terms: D000328:Adult; D000975:Antioxidants / Q000032:analysis* / Q000494:pharmacology; D001424:Bacterial Infections / Q000635:transmission; D001942:Breast Feeding / Q000009:adverse effects; D020013:Calcium Signaling / Q000187:drug effects; D002448:Cell Adhesion; D002449:Cell Aggregation; D003574:Cytochrome c Group / Q000378:metabolism; D016207:Cytokines / Q000032:analysis* / Q000494:pharmacology; D005260:Female; D006801:Humans; D007223:Infant; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1 / Q000032:analysis; D007781:Lactoferrin / Q000032:analysis; D008413:Mastitis / Q000276:immunology / Q000378:metabolism* / Q000473:pathology; D008894:Milk Proteins / Q000032:analysis* / Q000494:pharmacology; D008895:Milk, Human / Q000737:chemistry* / Q000166:cytology / Q000276:immunology; D009504:Neutrophils / Q000737:chemistry / Q000187:drug effects; D009895:Opsonin Proteins / Q000276:immunology; D010084:Oxidation-Reduction; D011188:Potassium / Q000032:analysis; D017472:Receptors, Interleukin-1 / Q000032:analysis; D018124:Receptors, Tumor Necrosis Factor / Q000032:analysis; D012795:Sialoglycoproteins / Q000032:analysis; D012964:Sodium / Q000032:analysis; D013211:Staphylococcus aureus / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000032:analysis
chemical_list: D000975:Antioxidants; D003574:Cytochrome c Group; D016207:Cytokines; C507763:IL1RN protein, human; D053590:Interleukin 1 Receptor Antagonist Protein; D007375:Interleukin-1; D008894:Milk Proteins; D009895:Opsonin Proteins; D017472:Receptors, Interleukin-1; D018124:Receptors, Tumor Necrosis Factor; D012795:Sialoglycoproteins; D014409:Tumor Necrosis Factor-alpha; D012964:Sodium; D007781:Lactoferrin; D011188:Potassium