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. 2026 Sep 22;16:1968526. doi: 10.3389/fcimb.2026.1968526

Figure 3.

Diagram illustrates the pathways of phage exposure and persistence, highlighting innate and adaptive immunity, experimental immune shielding, bacterial antiviral defense through CRISPR-Cas and anti-CRISPR systems, and elements of monitoring and feedback such as phage dose and antibody titer measurement.

Host immune barriers, bacterial antiviral defense, and monitoring strategies in pulmonary phage therapy. Phages enter via inhalation, intravenous, or oral routes and converge on a central “phage exposure and persistence” node. Five surrounding modules summarize the regulatory mechanisms in this chapter. (Upper-left, green) Innate immunity: complement C3b deposition opsonizes phages for clearance by macrophages and neutrophils. (Upper-right, purple) Adaptive immunity: BCR-driven B cells secrete anti-phage IgM/IgG, neutralizing phages and accelerating their clearance. (Lower-left, blue) Experimental immune shielding covers liposomal encapsulation, capsid engineering, and PD-L1 mimetic peptides (preclinical evidence only). (Lower-middle, orange) Bacterial antiviral defense: CRISPR-Cas restricts phage replication, while anti-CRISPR proteins protect the phage genome and restore replication. (Lower-right, gray) Monitoring and feedback: neutralizing antibody titer, complement activity, cytokine profile, and airway/blood phage titers inform adjustment of dose, frequency, route, and cocktail composition. A bottom bar summarizes that these combined strategies may prolong phage persistence and local antibacterial activity.