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. 2024 Nov 16;12(11):2341. doi: 10.3390/microorganisms12112341

Figure 4.

Figure 4

Pathway from bacterial invasion to blood clot: Bacterial cells release various components, including LPS, pathogen-associated molecular patterns (PAMPs), and outer membrane vesicles (OMVs), which can trigger an immune response. The invasion activates immune receptors such as CXCR2, CCR2, TLR-4/2, and NLRP3. This leads to an increase in inflammatory mediators, including IL-1β, IL-10, IL-17, Th17, IFN-γ, GM-CSF, G-CSF, IL-8, TNF-α, MCP1, and CRP. The immune response causes a reduction in nitric oxide (NO) levels and increases expression of endothelial adhesion molecules, such as E-selectin, ZO-1, vWF, PECAM-1, VCAM-1, and ICAM-1, disrupting endothelial function. Plaque formation involves oxidative stress, inflammatory cell infiltration, an imbalance in M1/M2 macrophage ratio, formation of foam cells, and lipid accumulation within the arterial wall. As plaque forms, factors like Cdc42 activation and increased collagen-binding proteins contribute to clotting. This leads to altered clotting and partial thromboplastin times, ultimately promoting thrombus (blood clot) formation [17]. Created with BioRender.com [31] (accessed on 29 October 2024).