Bacteria- and fungus-derived PAMPs induce innate immune memory via similar functional, metabolic, and transcriptional adaptations.

Autor:	McBride MA; Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, 1211 Medical Center Drive, Nashville 37232, Tennessee., Stothers CL; Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, 1211 Medical Center Drive, Nashville 37232, Tennessee., Fensterheim BA; Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, 1211 Medical Center Drive, Nashville 37232, Tennessee., Caja KR; Department of Anesthesiology, Vanderbilt University Medical Center, 1211 Medical Center Drive, Nashville 37232, Tennessee., Owen AM; Department of Anesthesiology, Vanderbilt University Medical Center, 1211 Medical Center Drive, Nashville 37232, Tennessee., Hernandez A; Department of Anesthesiology, Vanderbilt University Medical Center, 1211 Medical Center Drive, Nashville 37232, Tennessee., Bohannon JK; Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, 1211 Medical Center Drive, Nashville 37232, Tennessee.; Department of Anesthesiology, Vanderbilt University Medical Center, 1211 Medical Center Drive, Nashville 37232, Tennessee., Patil NK; Department of Anesthesiology, Vanderbilt University Medical Center, 1211 Medical Center Drive, Nashville 37232, Tennessee., Ali S; Department of Anesthesiology, Vanderbilt University Medical Center, 1211 Medical Center Drive, Nashville 37232, Tennessee., Dalal S; Department of Anesthesiology, Vanderbilt University Medical Center, 1211 Medical Center Drive, Nashville 37232, Tennessee., Rahim M; Department of Chemical and Biomolecular Engineering, Vanderbilt University, 2301 Vanderbilt Place, Nashville 37235, Tennessee., Trenary IA; Department of Chemical and Biomolecular Engineering, Vanderbilt University, 2301 Vanderbilt Place, Nashville 37235, Tennessee., Young JD; Department of Chemical and Biomolecular Engineering, Vanderbilt University, 2301 Vanderbilt Place, Nashville 37235, Tennessee.; Department of Molecular Physiology and Biophysics, Vanderbilt University, 2215 Garland Avenue, Nashville 37232, Tennessee., Williams DL; Department of Surgery, Quillen College of Medicine, East Tennessee State University, 325 North State of Franklin Road, Johnson City 37604, Tennessee.; Center for Inflammation, Infectious Disease and Immunity, Quillen College of Medicine, East Tennessee State University, 325 North State of Franklin Road, Johnson City 37604, Tennessee., Sherwood ER; Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, 1211 Medical Center Drive, Nashville 37232, Tennessee.; Department of Anesthesiology, Vanderbilt University Medical Center, 1211 Medical Center Drive, Nashville 37232, Tennessee.; Department of Surgery, Quillen College of Medicine, East Tennessee State University, 325 North State of Franklin Road, Johnson City 37604, Tennessee.; Center for Inflammation, Infectious Disease and Immunity, Quillen College of Medicine, East Tennessee State University, 325 North State of Franklin Road, Johnson City 37604, Tennessee.
Jazyk:	angličtina
Zdroj:	Journal of leukocyte biology [J Leukoc Biol] 2024 Jan 19; Vol. 115 (2), pp. 358-373.
DOI:	10.1093/jleuko/qiad120
Abstrakt:	Exposure to pathogen-associated molecular patterns (PAMPs) induces an augmented, broad-spectrum antimicrobial response to subsequent infection, a phenomenon termed innate immune memory. This study examined the effects of treatment with β-glucan, a fungus-derived dectin-1 ligand, or monophosphoryl lipid A (MPLA), a bacteria-derived Toll-like receptor 4 ligand, on innate immune memory with a focus on identifying common cellular and molecular pathways activated by these diverse PAMPs. Treatment with either PAMP prepared the innate immune system to respond more robustly to Pseudomonas aeruginosa infection in vivo by facilitating mobilization of innate leukocytes into blood, recruitment of leukocytes to the site of infection, augmentation of microbial clearance, and attenuation of cytokine production. Examination of macrophages ex vivo showed amplification of metabolism, phagocytosis, and respiratory burst after treatment with either agent, although MPLA more robustly augmented these activities and more effectively facilitated killing of bacteria. Both agents activated gene expression pathways in macrophages that control inflammation, antimicrobial functions, and protein synthesis and suppressed pathways regulating cell division. β-glucan treatment minimally altered macrophage differential gene expression in response to lipopolysaccharide (LPS) challenge, whereas MPLA attenuated the magnitude of the LPS-induced transcriptional response, especially cytokine gene expression. These results show that β-glucan and MPLA similarly augment the innate response to infection in vivo. Yet, MPLA more potently induces alterations in macrophage metabolism, antimicrobial functions, gene transcription and the response to LPS. Competing Interests: Conflict of interest None declared. (© The Author(s) 2023. Published by Oxford University Press on behalf of Society for Leukocyte Biology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)
Databáze:	MEDLINE
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