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Details

Autor(en) / Beteiligte
Titel
Brucella abortus induces mast cell activation through TLR-2 and TLR-4
Ist Teil von
  • Microbial pathogenesis, 2023-03, Vol.176, p.106005-106005, Article 106005
Ort / Verlag
England: Elsevier Ltd
Erscheinungsjahr
2023
Quelle
Access via ScienceDirect (Elsevier)
Beschreibungen/Notizen
  • The Gram-negative bacteria Brucella abortus is a major cause of brucellosis in animals and humans. The host innate immune response to B. abortus is mainly associated with phagocytic cells such as dendritic cells, neutrophils, and macrophages. However, as mast cells naturally reside in the main bacterial entry sites they may be involved in bacterial recognition. At present, little is known about the role of mast cells during B. abortus infection. The role of the innate immune receptors TLR2 and TLR4 in activation of mast cells by B. abortus (strain RB51) infection was analyzed in this study. The results showed that B. abortus did not induce mast cell degranulation, but did induce the synthesis of the cytokines IL-1β, IL-6, TNF-α, CCL3, CCL4, and CCL5. Furthermore, B. abortus stimulated key cell signaling molecules involved in mast cell activation such as p38 and NF-κB. Blockade of the receptors TLR2 and TLR4 decreased TNF-α and IL-6 release by mast cells in response to B. abortus. Taken together, our results demonstrate that mast cells are activated by B. abortus and may play a role in inducing an inflammatory response during the initial phase of the infection. Brucella abortus RB51 induces mast cell activation through TLR2 and TLR4, activating p-38 and p65 to produce proinflammatory cytokines and chemokines (created with BioRender.com). [Display omitted] . •Brucella abortus induce mast cell production of pro-inflammatory cytokines and chemokines.•Brucella abortus activates p38 and NF-kB cell signaling in mast cells.•The TLR-2 and TLR-4 participates in the recognition of Brucella abortus by mast cells.
Sprache
Englisch
Identifikatoren
ISSN: 0882-4010
eISSN: 1096-1208
DOI: 10.1016/j.micpath.2023.106005
Titel-ID: cdi_proquest_miscellaneous_2771334451

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