Neutrophil recruitment in endotoxin-induced murine mastitis is strictly dependent on mammary alveolar macrophages
| Autor: | Ayala Livneh-Kol, Sharon Elazar, Nahum Y. Shpigel, Erez Gonen, Ilan Rosenshine |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
Lipopolysaccharides
Adoptive cell transfer Lipopolysaccharide Neutrophils Interleukin-1beta Nitric Oxide Synthase Type II murine model 0403 veterinary science Mice chemistry.chemical_compound [SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB] Macrophage Mice Knockout 0303 health sciences [SDV.BA]Life Sciences [q-bio]/Animal biology lipopolysaccharide neutrophil 04 agricultural and veterinary sciences [SDV.MP]Life Sciences [q-bio]/Microbiology and Parasitology medicine.anatomical_structure Cytokines [SDV.IMM]Life Sciences [q-bio]/Immunology Female Original Article [SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC] lipids (amino acids peptides and proteins) Tumor necrosis factor alpha medicine.symptom Pulmonary alveolus Signal Transduction 040301 veterinary sciences Alveolar Epithelium Mice Inbred Strains Inflammation macrophage [SDV.BC]Life Sciences [q-bio]/Cellular Biology Biology mastitis 03 medical and health sciences Mammary Glands Animal medicine Animals Interleukin 8 030304 developmental biology General Veterinary Tumor Necrosis Factor-alpha Macrophages Interleukin-8 [SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biology Endotoxins Toll-Like Receptor 4 [SDV.GEN.GA]Life Sciences [q-bio]/Genetics/Animal genetics chemistry Immunology [SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologie |
| Zdroj: | Veterinary Research Veterinary Research, BioMed Central, 2010, 41 (1), ⟨10.1051/vetres/2009058⟩ |
| ISSN: | 1297-9716 0928-4249 |
| DOI: | 10.1051/vetres/2009058 |
| Popis: | International audience; Mastitis, inflammation of the mammary tissue, is a common disease in dairy animals and mammary pathogenic Escherichia coli (MPEC) is a leading cause of the disease. Lipopolysaccharide (LPS) is an important virulence factor of MPEC and inoculation of the mammary glands with bacterial LPS is sufficient to induce an inflammatory response. We previously showed using adoptive transfer of normal macrophages into the mammary gland of TLR4-deficient C3H/HeJ mice that LPS/TLR4 signaling on mammary alveolar macrophages is sufficient to elicit neutrophil recruitment into the alveolar space. Here we show that TLR4-normal C3H/HeN mice, depleted of alveolar macrophages, were completely refractory to LPS intramammary challenge. These results indicate that alveolar macrophages are both sufficient and essential for neutrophil recruitment elicited by LPS/TLR4 signaling in the mammary gland. Using TNFα gene-knockout mice and adoptive transfer of wild-type macrophages, we show here that TNFα produced by mammary alveolar macrophages in response to LPS/TLR4 signaling is an essential mediator eliciting blood neutrophil recruitment into the milk spaces. Furthermore, using the IL8 receptor or IL1 receptor gene-knockout mice we observed abrogated recruitment of neutrophils into the mammary gland and their entrapment on the basal side of the alveolar epithelium in response to intramammary LPS challenge. Adoptive transfer of wild-type neutrophils to IL1 receptor knockout mice, just before LPS challenge, restored normal neutrophil recruitment into the milk spaces. We conclude that neutrophil recruitment to the milk spaces is: (i) mediated through TNFα, which is produced by alveolar macrophages in response to LPS/TLR4 signaling and (ii) is dependent on IL8 and IL1β signaling and regulated by iNOS-derived NO. |
| Databáze: | OpenAIRE |
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