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Targeting Robo4-Dependent Slit Signaling to Survive the Cytokine Storm in Sepsis and Influenza
Journal article   Open access   Peer reviewed

Targeting Robo4-Dependent Slit Signaling to Survive the Cytokine Storm in Sepsis and Influenza

Nyall R. London, Weiquan Zhu, Fernando A. Bozza, Matthew C. P. Smith, Daniel M. Greif, Lise K. Sorensen, Luming Chen, Yuuki Kaminoh, Aubrey C. Chan, Samuel F. Passi, …
Science translational medicine, Vol.2(23), pp.23ra19-ra19
03/17/2010
DOI: 10.1126/scitranslmed.3000678
PMCID: PMC2875996
PMID: 20375003
url
https://www.ncbi.nlm.nih.gov/pmc/articles/2875996View
Open Access

Abstract

The innate immune system provides a first line of defense against invading pathogens by releasing multiple inflammatory cytokines, such as interleukin-1 beta and tumor necrosis factor-alpha, which directly combat the infectious agent and recruit additional immune responses. This exuberant cytokine release paradoxically injures the host by triggering leakage from capillaries, tissue edema, organ failure, and shock. Current medical therapies target individual pathogens with antimicrobial agents or directly either blunt or boost the host's immune system. We explored a third approach: activating with the soluble ligand Slit an endothelium-specific, Robo4-dependent signaling pathway that strengthens the vascular barrier, diminishing deleterious aspects of the host's response to the pathogen-induced cytokine storm. This approach reduced vascular permeability in the lung and other organs and increased survival in animal models of bacterial endotoxin exposure, polymicrobial sepsis, and H5N1 influenza. Thus, enhancing the resilience of the host vascular system to the host's innate immune response may provide a therapeutic strategy for treating multiple infectious agents.
Cell Biology Life Sciences & Biomedicine Medicine, Research & Experimental Research & Experimental Medicine Science & Technology

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