SOCS2 regulates alveolar bone loss in Aggregatibacter actinomycetemcomitans-induced periodontal disease
ConclusionsCollectively, data suggest that SOCS2 is a regulator ofAa-induced alveolar bone loss by controlling the differentiation and activity of bone cells, and proinflammatory cytokines availability in the periodontal microenvironment and an important target for new therapeutic strategies. Thus, it can be helpful in preventing alveolar bone loss in periodontal inflammatory conditions. (Source: Inflammation Research)
Source: Inflammation Research - March 13, 2023 Category: Research Source Type: research

Activating α7nAChR helps post-myocardial infarction healing by regulating macrophage polarization via the STAT3 signaling pathway
ConclusionActivating α7nAChR inhibits the early recruitment of pro-inflammatory monocytes/macrophages during MI and improves cardiac function and remodeling. Our findings suggest a promising therapeutic target for regulating monocyte/macrophage phenotypes and promoting healing after MI. (Source: Inflammation Research)
Source: Inflammation Research - March 13, 2023 Category: Research Source Type: research

A case of complete recovery in a hypereosinophilic dermatitis patient with dupilumab
ConclusionIn conclusion, we report a new application of dupilumab in HED patients, especially with  difficulties in reducing the glucocorticoid dose. (Source: Inflammation Research)
Source: Inflammation Research - March 13, 2023 Category: Research Source Type: research

Distinct cytokine profiles in patients with preeclampsia
ConclusionsThe set of cytokine profiles and risk assessment model described here can serve as a basis for developing early clinical diagnostic and therapeutic strategies for PE. (Source: Inflammation Research)
Source: Inflammation Research - March 12, 2023 Category: Research Source Type: research

Role of mitochondrial stress and the NLRP3 inflammasome in lung diseases
ConclusionThis review provides a resource for the discovery of new therapeutic mechanisms and suggests ideas for the development of new therapeutic drugs, thus promoting the rapid treatment of lung diseases. (Source: Inflammation Research)
Source: Inflammation Research - March 11, 2023 Category: Research Source Type: research

Non-canonical NLRC4 inflammasomes in astrocytes contribute to glioma malignancy
ConclusionThe findings of this study suggest that non-canonical NLRC4 inflammasomes contribute to poor prognosis in patients with glioma and induce an inflammatory microenvironment. We propose the pathological phenomenon of non-canonical NLRC4 inflammasomes and several therapeutic strategies based on the modulation of the inflammatory tumor microenvironment. (Source: Inflammation Research)
Source: Inflammation Research - March 10, 2023 Category: Research Source Type: research

Amnion-derived serum amyloid A1 participates in sterile inflammation of fetal membranes at parturition
ConclusionsSAA1 is a trigger of sterile inflammation of the fetal membranes at parturition. (Source: Inflammation Research)
Source: Inflammation Research - March 6, 2023 Category: Research Source Type: research

Blocking of programmed cell death-ligand 1 (PD-L1) expressed on endothelial cells promoted the recruitment of CD8+IFN- γ+ T cells in atherosclerosis
ConclusionsOur findings highlighted that blocking of PD-L1 promoted up-regulation of CD8  + IFN-γ + T cell-mediated immune responses, leading to the secretion of inflammatory cytokine that exacerbated the atherosclerotic burden and promoted inflammation. However, further studies are needed to gain insight into whether PD-L1 activation could be a novel immunotherapy strategy for atherosclerosis. (Source: Inflammation Research)
Source: Inflammation Research - March 3, 2023 Category: Research Source Type: research

Fructose malabsorption in ChREBP-deficient mice disrupts the small intestine immune microenvironment and leads to diarrhea-dominant bowel habit changes
ConclusionsThe collective data indicate that gut microbiome imbalance and disrupting homeostatic intestinal immune responses account for the development of gastrointestinal symptoms induced by fructose malabsorption. (Source: Inflammation Research)
Source: Inflammation Research - February 23, 2023 Category: Research Source Type: research

Screening inflammatory protein biomarkers on premature infants with necrotizing enterocolitis
ConclusionInflammatory proteins were different expressed in premature infants with NEC compared with controls or sepsis. Combining these proteins provide a higher diagnostic potential for preterm NEC infants. (Source: Inflammation Research)
Source: Inflammation Research - February 18, 2023 Category: Research Source Type: research

Correction to: Knockdown of lncRNA H19 alleviates ox ‑LDL‑induced HCAECs inflammation and injury by mediating miR‑20a‑5p/HDAC4 axis
(Source: Inflammation Research)
Source: Inflammation Research - February 18, 2023 Category: Research Source Type: research

The function of γδ T cells in humoral immune responses
ConclusionIn this review, we summarize current knowledge on how γδ T cells take part in the humoral immune response, which may assist future vaccine design. (Source: Inflammation Research)
Source: Inflammation Research - February 17, 2023 Category: Research Source Type: research

Retraction Note: Emerging protective roles of shengmai injection in septic cardiomyopathy in mice by inducing myocardial mitochondrial autophagy via caspase-3/Beclin-1 axis
(Source: Inflammation Research)
Source: Inflammation Research - February 16, 2023 Category: Research Source Type: research

RBM3 is associated with acute lung injury in septic mice and patients via the NF- κB/NLRP3 pathway
In conclusion, RBM3 was overexpressed in sepsis patients and LPS-induced mice. RBM3 gene deficiency aggravated s epsis-associated ALI through the NF-κB/NLRP3 pathway. (Source: Inflammation Research)
Source: Inflammation Research - February 13, 2023 Category: Research Source Type: research

Intestinal recruitment of CCR6-expressing Th17 cells by suppressing miR-681 alleviates endotoxemia-induced intestinal injury and reduces mortality
ConclusionThe results of the study indicate that control of intestinal Th17 cells by regulating novel miR-681/CCR6 signaling attenuates endotoxemia-induced intestinal injury. (Source: Inflammation Research)
Source: Inflammation Research - February 7, 2023 Category: Research Source Type: research