Sialoadhesin promotes rapid proinflammatory and type I IFN responses to a sialylated pathogen, Campylobacter jejuni

Area of Science:

• Immunology
• Microbiology
• Cell Biology

Background:

• Sialoadhesin (Sn) is a macrophage-specific receptor.
• Its role in pathogen interaction and immune response is not fully understood.

Purpose of the Study:

• To investigate the function of Sialoadhesin in macrophage interactions with sialylated pathogens.
• To elucidate the role of Sn in initiating inflammatory responses.

Main Methods:

• Utilized bone marrow-derived macrophages (BMDM) from wild-type and Sn-deficient mice.
• Employed heat-killed Campylobacter jejuni with sialylated glycans for in vitro and in vivo studies.
• Assessed phagocytosis, cytokine secretion (TNF-α, IL-6, IL-12, IL-10), and type I interferon (IFN-β) responses.

Main Results:

• Sn-deficient or non-binding BMDM showed significantly reduced phagocytosis of sialylated C. jejuni.
• MyD88-dependent secretion of key pro-inflammatory cytokines was diminished in the absence of functional Sn.
• In vivo, functional Sn was essential for rapid TNF-α and IFN-β responses to injected sialylated C. jejuni.
• Macrophages in the liver and spleen were identified as key sites for bacterial capture and immune response initiation.

Conclusions:

• Sialoadhesin is critical for the efficient capture of sialylated pathogens by macrophages.
• Sn engagement by pathogens triggers rapid pro-inflammatory and type I interferon responses.
• These findings highlight Sn as a key mediator in the innate immune system's defense against specific bacterial infections.