Innate immune cells, particularly macrophages and epithelial cells, play a key role in multiple layers of immune responses. Alarmins and pro-inflammatory cytokines from the IL (interleukin)-1 and TNF (tumour necrosis factor) families initiate the cascade of events by inducing chemokine release from bystander cells and by the up-regulation of adhesion molecules required for transendothelial trafficking of immune cells. Furthermore, innate cytokines produced by dendritic cells, macrophages, epithelial cells and innate lymphoid cells seem to play a critical role in polarization of helper T-cell cytokine profiles into specific subsets of Th1/Th2/Th17 effector cells or regulatory T-cells. Lastly, the innate immune system down-regulates effector mechanisms and restores homoeostasis in injured tissue via cytokines from the IL-10 and TGF (transforming growth factor) families mainly released from macrophages, preferentially the M2 subset, which have a capacity to induce regulatory T-cells, inhibit the production of pro-inflammatory cytokines and induce healing of the tissue by regulating extracellular matrix protein deposition and angiogenesis. Cytokines produced by innate immune cells represent an attractive target for therapeutic intervention, and multiple molecules are currently being tested clinically in patients with inflammatory bowel disease, rheumatoid arthritis, systemic diseases, autoinflammatory syndromes, fibrosing processes or malignancies. In addition to the already widely used blockers of TNFα and the tested inhibitors of IL-1 and IL-6, multiple therapeutic molecules are currently in clinical trials targeting TNF-related molecules [APRIL (a proliferation-inducing ligand) and BAFF (B-cell-activating factor belonging to the TNF family)], chemokine receptors, IL-17, TGFβ and other cytokines.

Cytokine networking of innate immunity cells: a potential target of therapy.

The endothelium plays a crucial role in inflammation. A balanced control of inflammation requires the action of glucocorticoids (GCs), steroidal hormones with potent cell-specific anti-inflammatory properties. Besides the classic anti-inflammatory effects of GCs on leukocytes, recent studies confirm that endothelial cells also represent an important target for GCs. GCs regulate different aspects of endothelial physiology including expression of adhesion molecules, production of pro-inflammatory cytokines and chemokines, and maintenance of endothelial barrier integrity. However, the regulation of endothelial GC sensitivity remains incompletely understood. In this review, we specifically examine the endothelial response to GCs in various inflammatory diseases ranging from multiple sclerosis, stroke, sepsis, and vasculitis to atherosclerosis. Shedding more light on the cross talk between GCs and endothelium will help to improve existing therapeutic strategies and develop new therapies better tailored to the needs of patients.

/pdf/endothelial-response-to-glucocorticoids-in-inflammatory-12jq988mnq.pdf

Endothelial Response to Glucocorticoids in Inflammatory Diseases.

The neutrophilic dermatoses (ND) may present with pustules, plaques, ulcerations, and general malaise They are secondary to the invasion of the skin by normal polymorphonuclear leukocytes in the absence of infection ND are often associated with particular systemic diseases The management of affected patients is reviewed, with a focus on nursing care

The neutrophilic dermatoses.

Tumor necrosis factor- (TNF-) like weak inducer of apoptosis (TWEAK) participates in multiple biological activities via binding to its sole receptor-fibroblast growth factor-inducible 14 (Fn14). The TWEAK/Fn14 signaling pathway is activated in skin inflammation and modulates the inflammatory responses of keratinocytes by activating nuclear factor-κB signals and enhancing the production of several cytokines, including interleukins, monocyte chemotactic protein-1, RANTES (regulated on activation, normal T cell expressed and secreted), and interferon gamma-induced protein 10. Mild or transient TWEAK/Fn14 activation contributes to tissular repair and regeneration while excessive or persistent TWEAK/Fn14 signals may lead to severe inflammatory infiltration and tissue damage. TWEAK also regulates cell fate of keratinocytes, involving the function of Fn14-TNF receptor-associated factor-TNF receptor axis. By recruiting inflammatory cells, promoting cytokine production, and regulating cell fate, TWEAK/Fn14 activation plays a pivotal role in the pathogenesis of various skin disorders, such as psoriasis, atopic dermatitis, cutaneous vasculitis, human papillomavirus infection and related skin tumors, and cutaneous autoimmune diseases. Therefore, the TWEAK/Fn14 pathway may be a potential target for the development of novel therapeutics for skin inflammatory diseases.

https://downloads.hindawi.com/journals/mi/2017/6746870.pdf

TWEAK/Fn14 Activation Participates in Skin Inflammation

Pulmonary microvascular leakage is one of the characteristics of blood–air barrier dysfunction in septic acute lung injury/acute respiratory distress syndrome (ALI/ARDS). Fibroblast growth factor-inducible 14 (Fn14) exerts diverse functions under certain circumstances. However, the role of F

FN14 Blockade on Pulmonary Microvascular Endothelial Cells Improves the Outcome of Sepsis-Induced Acute Lung Injury.

Abstract IL-33, which is a crucial modulator of adaptive immune responses far beyond type 2 response, can enhance the function of several T cell subsets and maintain the immune homeostasis. However, the contribution of IL-33 to double negative T (DNT) cell remains unappreciated. Here, we demonstrated that the IL-33 receptor ST2 was expressed on DNT cells, and that IL-33 stimulation increased DNT cells proliferation and survival in vivo and in vitro. Transcriptome sequencing analysis also demonstrated that IL-33 enhanced the biological function of DNT cells, especially effects on proliferation and survival. IL-33 promoted DNT cells survival by regulating Bcl-2, Bcl-xl and Survivin expression. IL-33-TRAF4/6-NF-κB axis activation promoted the transmission of essential division and survival signals in DNT cells. However, IL-33 failed to enhance the expression of immunoregulatory molecules in DNT cells. DNT cells therapy combined with IL-33 inhibited T cells survival and further ameliorated ConA-induced liver injury, which mainly depended on the proliferative effect of IL-33 on DNT cells in vivo. Finally, we stimulated human DNT cells with IL-33, and similar results were observed. In conclusion, we revealed a cell intrinsic role of IL-33 in the regulation of DNT cells, thereby identifying a previously unappreciated pathway supporting the expansion of DNT cells in the immune environment. 

/pdf/il-33-promotes-double-negative-t-cell-survival-via-the-nf-kb-tbdn7k1l.pdf

IL-33 promotes double negative T cell survival via the NF-κB pathway

High-resolution mass spectrometry assay for quantifying ceramides and dihydroceramides in the cerebrospinal fluid from patients who experienced intracranial infection after craniotomy.

Background Scar recovery in elderly burn patients is essential for wound healing and psychological well-being. Total glycosides from Centella asiatica have gained attention for their anti-inflammatory, antioxidant, and wound-healing properties, showing promise in burn care. Objectives This study investigates the synergistic effects of combined nursing interventions and Asiaticosides on scar recovery and psychological well-being in patients undergoing scald scar repair. The pharmacological properties of these glycosides, including their anti-inflammatory, anti-oxidant, and wound-healing potential, are explored in the context of clinical care to enhance patient outcomes. Materials and Methods A cohort of 184 patients treated for scald scars between April 2023 and April 2024 was divided into two groups: an observation group receiving combined nursing interventions with Asiaticosides, and a comparison group receiving standard care. Scar assessment was conducted using the Vancouver Scar Scale (VSS), pain was measured by the Visual Analogue Scale (VAS), and psychological states were evaluated using the Self-rating Anxiety Scale (SAS) and Self-rating Depression Scale (SDS). Results Statistically significant improvements were observed in the observation group, including reduced VSS and VAS scores, as well as enhanced psychological states, compared to the control group (p < 0.05). The glycosides facilitated faster scar healing, reduced inflammation, and improved overall patient well-being. Conclusion Asiaticosides exhibit promising therapeutic potential in enhancing scar recovery and psychological health in elderly scald patients when combined with comprehensive nursing care. Further research into their mechanisms may solidify their role in integrated scald injury management.

Effects of Asiaticosides on Scar Recovery and Psychological Well-being in Patients with Scald Injuries

In 1964, Sweet described an acute febrile neutrophilic dermatosis. It is now widely accepted that Sweet syndrome is one of the associated neutrophilic dermatoses. Herein, we describe an unusual case of Sweet syndrome in a 5-year-old child who suffered from recurrent papules, plaques, and blisters on his face and trunk after the initial onset of fever without an obvious cause. Two skin biopsies were performed. The histopathological findings of the left arm biopsy showed a subepidermal blister with dense infiltrating neutrophils within the blister that were superficial to the middle layer of the dermis. The biopsy from a plaque on the left leg showed a dense infiltrate of neutrophils and a large number of infiltrating histiocytes superficial to the middle layer of the dermis. Direct immunofluorescence of a skin biopsy from the left arm confirmed that immunoglobulin M (IgM), IgG, IgA, and C3 expression were negative.

An unusual case of Sweet syndrome in a child: overlapping presentation with erythema elevatum diutinum.

Our previous work indicated that TWEAK is associated with various types of cutaneous vasculitis (CV). Herein, we investigate the effects of TWEAK on vascular injury and adhesion molecule expression in CV mice. We showed that TWEAK priming in mice induced a local CV. Furthermore, TWEAK priming also increased the extravasation of FITC-BSA, myeloperoxidase activity and the expression of E-selectin and ICAM-1. Conversely, TWEAK blockade ameliorated the LPS-induced vascular damage, leukocyte infiltrates and adhesion molecules expression in LPS-induced CV. In addition, TWEAK treatment of HDMECs up-regulated E-selectin and ICAM-1 expression at both mRNA and protein levels. TWEAK also enhanced the adhesion of PMNs to HDMECs. Finally, western blot data revealed that TWEAK can induce phosphorylation of p38, JNK and ERK in HDMECs. These data suggest that TWEAK acted as an inducer of E-selectin and ICAM-1 expression in CV mice and HDMECs, may contribute to the development of CV.

/pdf/tweak-enhances-e-selectin-and-icam-1-expression-and-may-5ca7xn2gur.pdf

TWEAK Enhances E-selectin and ICAM-1 Expression, and May Contribute to the Development of Cutaneous Vasculitis

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