4.5 Article

Stabilin-1 plays a protective role against Listeria monocytogenes infection through the regulation of cytokine and chemokine production and immune cell recruitment

期刊

VIRULENCE
卷 12, 期 1, 页码 2088-2103

出版社

TAYLOR & FRANCIS INC
DOI: 10.1080/21505594.2021.1958606

关键词

Listeria; scavenger receptors; STAB-1; innate immunity; infection

资金

  1. National Funds through FCT-Fundacao para a Ciencia e a Tecnologia, I.P. [UIDB/04293/2020]
  2. FCT [SFRH/BD/89542/2012, SFRH/BD/86871/2012]
  3. Fundacao para a Ciencia e a Tecnologia [UIDB/04293/2020]
  4. i3S Scientific Platforms: Advanced Light Microscopy, member of the national infrastructure PPBI-Portuguese Platform of BioImaging [POCI-01-0145-FEDER-022122]
  5. Fundação para a Ciência e a Tecnologia [SFRH/BD/89542/2012, SFRH/BD/86871/2012] Funding Source: FCT

向作者/读者索取更多资源

STAB-1 plays a regulatory role in the immune response and bacterial clearance during Lm infection, as well as in modulating bacterial uptake by macrophages.
Scavenger receptors are part of a complex surveillance system expressed by host cells to efficiently orchestrate innate immune response against bacterial infections. Stabilin-1 (STAB-1) is a scavenger receptor involved in cell trafficking, inflammation, and cancer; however, its role in infection remains to be elucidated. Listeria monocytogenes (Lm) is a major intracellular human food-borne pathogen causing severe infections in susceptible hosts. Using a mouse model of infection, we demonstrate here that STAB-1 controls Lm-induced cytokine and chemokine production and immune cell accumulation in Lm-infected organs. We show that STAB-1 also regulates the recruitment of myeloid cells in response to Lm infection and contributes to clear circulating bacteria. In addition, whereas STAB-1 appears to promote bacterial uptake by macrophages, infection by pathogenic Listeria induces the down regulation of STAB-1 expression and its delocalization from the host cell membrane. We propose STAB-1 as a new SR involved in the control of Lm infection through the regulation of host defense mechanisms, a process that would be targeted by bacterial virulence factors to promote infection.

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