The role of interleukin-1 in general pathology

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Abstract

Interleukin-1, an inflammatory cytokine, is considered to have diverse physiological functions and pathological significances and play an important role in health and disease. In this decade, interleukin-1 family members have been expanding and evidence is accumulating that highlights the importance of interleukin-1 in linking innate immunity with a broad spectrum of diseases beyond inflammatory diseases. In this review, we look back on the definition of “inflammation” in traditional general pathology and discuss new insights into interleukin-1 in view of its history and the molecular bases of diseases, as well as current progress in therapeutics.

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Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death.

Jianjin Shi, Yue Zhao, Kun Wang … (2015)

Inflammatory caspases (caspase-1, -4, -5 and -11) are critical for innate defences. Caspase-1 is activated by ligands of various canonical inflammasomes, and caspase-4, -5 and -11 directly recognize bacterial lipopolysaccharide, both of which trigger pyroptosis. Despite the crucial role in immunity and endotoxic shock, the mechanism for pyroptosis induction by inflammatory caspases is unknown. Here we identify gasdermin D (Gsdmd) by genome-wide clustered regularly interspaced palindromic repeat (CRISPR)-Cas9 nuclease screens of caspase-11- and caspase-1-mediated pyroptosis in mouse bone marrow macrophages. GSDMD-deficient cells resisted the induction of pyroptosis by cytosolic lipopolysaccharide and known canonical inflammasome ligands. Interleukin-1β release was also diminished in Gsdmd(-/-) cells, despite intact processing by caspase-1. Caspase-1 and caspase-4/5/11 specifically cleaved the linker between the amino-terminal gasdermin-N and carboxy-terminal gasdermin-C domains in GSDMD, which was required and sufficient for pyroptosis. The cleavage released the intramolecular inhibition on the gasdermin-N domain that showed intrinsic pyroptosis-inducing activity. Other gasdermin family members were not cleaved by inflammatory caspases but shared the autoinhibition; gain-of-function mutations in Gsdma3 that cause alopecia and skin defects disrupted the autoinhibition, allowing its gasdermin-N domain to trigger pyroptosis. These findings offer insight into inflammasome-mediated immunity/diseases and also change our understanding of pyroptosis and programmed necrosis.

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Origin and physiological roles of inflammation.

Ruslan Medzhitov (2008)

Inflammation underlies a wide variety of physiological and pathological processes. Although the pathological aspects of many types of inflammation are well appreciated, their physiological functions are mostly unknown. The classic instigators of inflammation - infection and tissue injury - are at one end of a large range of adverse conditions that induce inflammation, and they trigger the recruitment of leukocytes and plasma proteins to the affected tissue site. Tissue stress or malfunction similarly induces an adaptive response, which is referred to here as para-inflammation. This response relies mainly on tissue-resident macrophages and is intermediate between the basal homeostatic state and a classic inflammatory response. Para-inflammation is probably responsible for the chronic inflammatory conditions that are associated with modern human diseases.

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Cancer-related inflammation.

Alberto Mantovani, Paola Allavena, Antonio Sica … (2008)

The mediators and cellular effectors of inflammation are important constituents of the local environment of tumours. In some types of cancer, inflammatory conditions are present before a malignant change occurs. Conversely, in other types of cancer, an oncogenic change induces an inflammatory microenvironment that promotes the development of tumours. Regardless of its origin, 'smouldering' inflammation in the tumour microenvironment has many tumour-promoting effects. It aids in the proliferation and survival of malignant cells, promotes angiogenesis and metastasis, subverts adaptive immune responses, and alters responses to hormones and chemotherapeutic agents. The molecular pathways of this cancer-related inflammation are now being unravelled, resulting in the identification of new target molecules that could lead to improved diagnosis and treatment.

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Author and article information

Contributors

Junya Masumoto:

ORCID: http://orcid.org/0000-0003-0847-0456

+81-89-960-5977 , masumoto@m.ehime-u.ac.jp

Journal

Journal ID (nlm-ta): Inflamm Regen

Journal ID (iso-abbrev): Inflamm Regen

Title: Inflammation and Regeneration

Publisher: BioMed Central (London )

ISSN (Print): 1880-9693

ISSN (Electronic): 1880-8190

Publication date (Electronic): 6 June 2019

Publication date PMC-release: 6 June 2019

Publication date Collection: 2019

Volume: 39

Electronic Location Identifier: 12

Affiliations

ISNI 0000 0001 1011 3808, GRID grid.255464.4, Department of Pathology, , Ehime University Graduate School of Medicine and Proteo-Science Center, ; Shitsukawa 454, Toon, Ehime 791-0295 Japan

Author information

Junya Masumoto http://orcid.org/0000-0003-0847-0456

Article

Publisher ID: 101

DOI: 10.1186/s41232-019-0101-5

PMC ID: 6551897

PubMed ID: 31182982

SO-VID: ee82d063-8788-4ad8-9804-63551517ace8

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 3 March 2019

Date accepted : 7 May 2019

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Keywords: interleukin-1,metabolic inflammation,inflammatory diseases,cancer,drug target

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Keywords: interleukin-1, metabolic inflammation, inflammatory diseases, cancer, drug target

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The role of interleukin-1 in general pathology

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Cancer Immunotherapy

Most cited references 223

Cleavage of GSDMD by inflammatory caspases determines pyroptotic cell death.

Origin and physiological roles of inflammation.

Cancer-related inflammation.

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