Fig. 8: Illustration of the impact of SPARCL1 on the progression of influenza pneumonia. | Nature Communications

Fig. 8: Illustration of the impact of SPARCL1 on the progression of influenza pneumonia.

From: Vascular endothelial-derived SPARCL1 exacerbates viral pneumonia through pro-inflammatory macrophage activation

Fig. 8

In influenza pneumonia, SPARCL1 from endothelial cells enters the alveoli via damaged blood vessels, prompting alveolar macrophages to adopt a pro-inflammatory (M1-like) state. This transformation hinges on SPARCL1 inducing TLR-4/NF-κB signaling activation in alveolar macrophages, leading to increased expression of pro-inflammatory cytokines. Simultaneously, heightened CCL-2 attracts more monocytes and macrophages into the alveoli. These recruited macrophages, once again exposed to SPARCL1 within the alveoli, further adopt a pro-inflammatory phenotype. The cumulative effect intensifies the local inflammatory response, causing tissue damage and hindering lung repair. Schematics and icons created with BioRender.com.

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