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. 2020 Dec 10;16(12):e1009054. doi: 10.1371/journal.ppat.1009054

Fig 1. Bacterial modulation of neutrophil degranulation.

Fig 1

Several pathogens either induce or inhibit neutrophil degranulation to promote infection. Uptake of Mycobacteria by CR3 passively prevents fusion of granules with the phagosome. Chlamydia produces CPAF, which cleaves FPR2 to inhibit degranulation. Yersinia injects effectors via the type III secretion system to inhibit degranulation, and Neisseria that does not display Opa reduces fusion of neutrophil granules with the phagosome. On the other hand, Filifactor alocis induces TLR2 signaling, triggering degranulation. Staphylococcus aureus produces PSMs, of which PSMα4 stimulates degranulation through FPR2. Streptococcal species that produce M protein also induce neutrophil degranulation by complexing with fibrinogen and binding β1 integrins. Finally, Anaplasma phagocytophilum induces neutrophil degranulation, although the exact mechanism remains unknown. CPAF, chlamydial protease-like activity factor; CR3, complement receptor 3; FPR2, N-formyl peptide receptor 2; Opa, opacity-associated protein; PSM, phenol-soluble modulin; TLR2, Toll-like receptor 2.