From the Guidelines

Yes, Interleukin-1 beta (IL-1β) and Interleukin-18 (IL-18) can cause bone marrow inflammation.

IL-18 is a proinflammatory cytokine that plays a crucial role in the pathogenesis of Still's disease, which is characterized by bone marrow inflammation 1.
Elevated levels of IL-18 have been observed in patients with Still's disease, and it is believed to initiate the inflammatory cascade that includes other cytokines such as IFN-γ, IL-6, and TNF-α 1.
IL-1β is also a proinflammatory cytokine that is involved in the pathogenesis of Still's disease, although its role is not as well-defined as IL-18 1.
The diagnosis of Still's disease relies on a combination of clinical and biological findings, including elevated levels of IL-18 and other biomarkers such as S100 proteins and ferritin 1.
Novel diagnostic biomarkers, including IL-18, have been investigated to improve the diagnosis of macrophage activation syndrome (MAS), a life-threatening complication of Still's disease 1.

IL-18: elevated levels are suggestive of predisposition to the development of MAS in the sJIA population 1.
S100 proteins: elevated levels are associated with Still's disease and can be used as diagnostic biomarkers 1.
Ferritin: elevated levels are associated with Still's disease, but its specificity is lower than IL-18 and S100 proteins 1.

Early diagnosis and treatment of Still's disease are crucial to prevent long-term complications, including bone marrow inflammation and MAS.
The use of IL-18 and other biomarkers can help improve the diagnosis of Still's disease and MAS, allowing for earlier initiation of treatment.
Further research is needed to fully understand the role of IL-1β and IL-18 in the pathogenesis of Still's disease and to develop more effective treatments for this condition.

From the Research

IL-1β and IL-18 are members of the IL-1 family and play a crucial role in regulating inflammation 2, 3, 4
These cytokines can be secreted from immune cells via unconventional pathways and can operate in the absence of complete cell lysis and cell death 2
IL-1β and IL-18 share a common secretory pathway that depends upon membrane permeability 2

Deletion of Il1b (IL-1β) in Nlrc4-transgenic mice reduced bone marrow hyperplasia, while mice deficient in Il18 (IL-18) showed no bone marrow hyperplasia 5
This suggests that IL-1β, but not IL-18, plays a role in bone marrow inflammation in the context of NLRC4-induced autoinflammation 5
Blocking IL-1 activity, including IL-1β, has been shown to be beneficial in reducing disease severity in various inflammatory syndromes, including those affecting the bone marrow 6

IL-1β and IL-18 are processed by caspase 1 to their biologically active mature forms 3, 4
These cytokines bind to their specific receptors, leading to the activation of NF-kB and the induction of inflammatory mediators 3
IL-1β and IL-18 can contribute to the elevation of markers of inflammation, such as IL-6, serum amyloid A, and C-reactive protein 4