Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Inflammasomes can prevent systemic dissemination of enteropathogenic bacteria. As adapted pathogens including Salmonella Typhimurium (S. Tm) have evolved evasion strategies, it has remained unclear when and where inflammasomes restrict their dissemination. Bacterial population dynamics establish that the NAIP/NLRC4 inflammasome specifically restricts S. Tm migration from the gut to draining lymph nodes. This is solely attributable to NAIP/NLRC4 within intestinal epithelial cells (IECs), while S. Tm evades restriction by phagocyte NAIP/NLRC4. NLRP3 and Caspase-11 also fail to restrict S. Tm mucosa traversal, migration to lymph nodes, and systemic pathogen growth. The ability of IECs (not phagocytes) to mount a NAIP/NLRC4 defense in vivo is explained by particularly high NAIP/NLRC4 expression in IECs and the necessity for epithelium-invading S. Tm to express the NAIP1-6 ligands-flagella and type-III-secretion-system-1. Imaging reveals both ligands to be promptly downregulated following IEC-traversal. These results highlight the importance of intestinal epithelial NAIP/NLRC4 in blocking bacterial dissemination in vivo, and explain why this constitutes a uniquely evasion-proof defense against the adapted enteropathogen S. Tm.

Original publication

DOI

10.1038/s41385-019-0247-0

Type

Journal article

Journal

Mucosal Immunol

Publication Date

05/2020

Volume

13

Pages

530 - 544

Keywords

Animals, CARD Signaling Adaptor Proteins, Calcium-Binding Proteins, Caspases, Disease Models, Animal, Host-Pathogen Interactions, Humans, Intestinal Mucosa, Lymphoid Tissue, Mice, Mice, Knockout, NLR Family, Pyrin Domain-Containing 3 Protein, Neuronal Apoptosis-Inhibitory Protein, Organ Specificity, Pathogen-Associated Molecular Pattern Molecules, Phagocytes, Salmonella Infections, Salmonella typhimurium