Mitigating Viral Impact on the Radiation Response of the Lung

• DOI: 10.1667/rade-24-00103.1
• Publication Date: 2024-07-25T00:01:48Z
• Authors: Angela M. Groves; Nicole D. Paris; Carl J. Johnston; Eric Hernady; Jacob Finkelstein; Paige Lawrence; Brian Marples
• Keywords: Proinflammatory cytokine

Inflammation is a key factor in both influenza and radiation-induced lung pathophysiology. This implies commonality of response to pulmonary damage from these insults suggests exacerbated pathology may occur after combined exposure. We therefore tested the hypothesis that past inflammation viral infection alters microenvironment lowers tolerance for radiation injury. Mice were inoculated with A virus (IAV) three weeks later, clearance, mice received total-body irradiation (TBI). Survival as well systemic local assessed, strategies mitigate injury investigated. After IAV alone, body condition recovered within 3 weeks, however inflammatory pathways remained active 15 weeks. subsequent TBI responses, evident by increased lethality, enhanced histologically an altered macrophage phenotype. To this sensitivity, captopril [an angiotensin converting enzyme inhibitor (ACEi)] was administered limit tissue inflammation, or monocyte-derived recruitment blocked C-C chemokine receptor type 2 (CCR2) inhibitor. Both treatments abrogated changes circulating immune cells observed 4 TBI, attenuated pro-inflammatory phenotypes alveolar macrophages, appearing shift cell dynamics towards recovery. Histologically apparent not improved either treatment. show latent exacerbates morbidity mortality. Although attenuate proinflammatory can normalize dynamics, does fully Recognizing infections enhance radiosensitivity critical importance patients receiving it could increase incidence adverse outcomes.