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. 2022 May 18;4(5):e0699. doi: 10.1097/CCE.0000000000000699

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Copyright © 2022 The Authors. Published by Wolters Kluwer Health, Inc. on behalf of the Society of Critical Care Medicine.

This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially without permission from the journal.

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Figure 1. — Surfactant protein D (SPD) deficiency reduces Escherichia coli bacteremia and mortality after cecal ligation and puncture (CLP) by reducing cecal colonization by E. coli. A, CLP (100 % ligation, 19-G puncture, two holes) was performed on SPD^+/+ and SPD^−/− mice (n = 16/group) (Gehan-Breslow-Wilcoxon, *p < 0.05). B, Blood E. coli load following CLP. E. coli colony forming units (CFU) in blood 24 hr after CLP (100% ligation, 19-G puncture, one hole) in SPD^+/+ (n = 9) and SPD^−/− (n = 18) mice (Mann-Whitney, ****p < 0.0001). C, Ex vivo phagocytosis. Neutrophils were isolated from SPD^+/+ and SPD^−/− mice (n = 3/group) and incubated with green fluorescent protein (GFP) expressing E. coli. The percentage of GFP+ cells was determined by flow cytometry (p > 0.05, Mann-Whitney). D, In vivo phagocytosis. SPD^+/+ mice (n = 5–6) and SPD^−/− mice (n = 6) were injected intraperitoneally with GFP expressing E. coli. Neutrophils and macrophages were identified by cell surface markers, and the percentage of GFP+ cells was determined by flow cytometry (p > 0.05, Mann-Whitney). E, Post E. Coli fibrin clot survival of SPD^+/+ and SPD^−/− mice (n = 9/group) (Gehan-Breslow-Wilcoxon, p > 0.05), where both SPD^+/+ and SPD^−/− mice were exposed to exogenous E. coli. E. coli for fibrin clot was isolated from SPD^+/+ cecum.