https://journal.chestnet.org/article/S0012-3692(16)38415-X/pdf

Definitions for Sepsis and Organ Failure and Guidelines for the Use of Innovative Therapies in Sepsis

Atherosclerosis, the principal cause of heart attack, stroke and gangrene of the extremities, is responsible for 50% of all mortality in the USA, Europe and Japan. The lesions result from an excessive, inflammatory-fibroproliferative response to various forms of insult to the endothelium and smooth muscle of the artery wall. A large number of growth factors, cytokines and vasoregulatory molecules participate in this process. Our ability to control the expression of genes encoding these molecules and to target specific cell types provides opportunities to develop new diagnostic and therapeutic agents to induce the regression of the lesions and, possibly, to prevent their formation.

The pathogenesis of atherosclerosis: a perspective for the 1990s

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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Cancer-related inflammation.

Objective:To provide an update to the “Surviving Sepsis Campaign Guidelines for Management of Severe Sepsis and Septic Shock,” last published in 2008.Design:A consensus committee of 68 international experts representing 30 international organizations was convened. Nominal groups were assembled at ke

Surviving sepsis campaign: international guidelines for management of severe sepsis and septic shock: 2012.

Abundant data link hypercholesterolaemia to atherogenesis. However, only recently have we appreciated that inflammatory mechanisms couple dyslipidaemia to atheroma formation. Leukocyte recruitment and expression of pro-inflammatory cytokines characterize early atherogenesis, and malfunction of inflammatory mediators mutes atheroma formation in mice. Moreover, inflammatory pathways promote thrombosis, a late and dreaded complication of atherosclerosis responsible for myocardial infarctions and most strokes. The new appreciation of the role of inflammation in atherosclerosis provides a mechanistic framework for understanding the clinical benefits of lipid-lowering therapies. Identifying the triggers for inflammation and unravelling the details of inflammatory pathways may eventually furnish new therapeutic targets.

Inflammation in atherosclerosis

The subject invention concerns a nucleic acid comprising a nucleotide sequence encoding human interleukin-1 (IL-1), and fragments thereof, and the polypeptides and peptides obtained. Specifically, the subject invention comprises the cloning of a cDNA synthesized by reverse transcription of poly(A)RNA isolated from adherent human monocytes stimulated with bacterial endotoxin. The subject invention further concerns antibodies that are immunoreactive with human IL-1β proteins. Human IL-1 is useful to induce the production of IL-2 by activated T-cells; it also acts on B-cells and NK-cells.

Antibodies to IL-1β

Interleukin 1 as mediator of the acute-phase response.

The inhibition of the biological activity of IL‐1 by recombinant human IL‐1 receptor antagonist (IL‐1ra) has been investigated in several, controlled clinical trials. Encouraging results have been reported, in particular in patients with rheumatoid arthritis. In the present study, we investigated the influence of treatment of wild type mice with IL‐1ra, which resulted in an incomplete and transient inhibition of IL‐1 activity. Treatment with recombinant human IL‐1ra resulted in an enhanced bacterial outgrowth in the lungs of BALB\c and C57BL\6 mice early after induction of pneumococcal pneumonia, without influencing survival or the pulmonary inflammatory response. The effect of IL‐1ra on the host response to S. pneumoniae pneumonia is modest and transient. The present data, together with the findings in IL‐1R\ mice in earlier work, suggest that IL‐1 occupies a role in the pulmonary immune response to S. pneumoniae that is substantially less prominent than that of TNF‐α.

Interleukin‐1 receptor antagonist transiently impairs antibacterial defense but not survival in murine pneumococcal pneumonia

The subject invention concerns a nucleic acid comprising a nucleotide sequence encoding human interleukin-1 (IL-1), and fragments thereof, and the polypeptides and peptides obtained Specifically, the subject invention comprises the cloning of a cDNA synthesized by reverse transcription of poly(A)RNA isolated from adherent human monocytes-stimulated with bacterial endotoxin Human IL-1 is useful to induce the production of IL-2 by activated T-cells; it also acts on B-cells and NK-cells

IL-1βprotein precursor

INTRODUCTION Hairy cell leukemia (HCL) is a rare, B cell derived neoplasia, characterized by the presence of distinctive lymphoid cells in the bone marrow, spleen and liver. It is most often associated with splenomegaly and bone marrow insufficiency [1, 2]. Circulating cytokines may play a possible role in the development of clinical features in HCL, and there is also evidence that the growth of hairy cells may be regulated [...]

Charles A. Dinarello

Papers

Antibodies to IL-1β

Interleukin 1 as mediator of the acute-phase response.

Interleukin‐1 receptor antagonist transiently impairs antibacterial defense but not survival in murine pneumococcal pneumonia

IL-1βprotein precursor

Correlation of serum levels of interleukin-1 family members with disease activity and response to treatment in hairy cell leukemia