1. Pseudomonas aeruginosa Pneumonia Causes a Loss of Type-3 and an Increase in Type-1 Innate Lymphoid Cells in the Gut.
- Author
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Fuchs A, Ghosh S, Chang SW, Bochicchio GV, and Turnbull IR
- Subjects
- Animals, Male, Mice, Inbred C57BL, Pneumonia, Bacterial complications, Pseudomonas Infections complications, Mice, Intestinal Mucosa immunology, Lymphocytes, Pneumonia, Bacterial immunology, Pseudomonas Infections immunology, Sepsis immunology
- Abstract
Background: Sepsis induces gut barrier dysfunction characterized by increased gut epithelial apoptosis and increased intestinal permeability. The cytokine IL-22 has been demonstrated to regulate gut barrier function. Type-3 innate lymphoid cells (ILC3) are the predominate source of IL-22 in the GI tract. We hypothesized that sepsis may cause changes to the gut ILC3/IL-22 axis., Materials and Methods: Sepsis was induced in WT and IL-22 KO mice by Pseudomonas aeruginosa pneumonia. Changes in gut-associated leukocyte populations were determined by flow-cytometry and ILC-associated transcripts were measured by RT-PCR. The effect of sepsis on gut permeability, pulmonary microbial burden, gut epithelial apoptosis, and survival was compared between WT and IL-22-/- mice., Results: Sepsis resulted in a significant decrease in the number of ILC3 in the gut, with a reciprocal increase in type-1 ILC (ILC1). Consistent with prior reports, sepsis was associated with increased gut permeability; however there was no difference in gut permeability, gut epithelial apoptosis, pulmonary microbial burden, or survival between WT and IL-22-/- mice., Conclusions: Septic pneumonia causes a decrease in gut-associated ILC3 and an associated reciprocal increase in ILC1. This may reflect inflammation-induced conversion of ILC3 to ILC1. Constitutive systemic IL-22 deficiency does not alter sepsis-induced gut barrier dysfunction., Competing Interests: Decleration of competing interest The authors declare no conflict of interest., (Copyright © 2021 Elsevier Inc. All rights reserved.)
- Published
- 2021
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