G-CSF Clone 'SPM468 antibody Host Rat
- Known as:
- G-CSF Clone 'SPM468 (anti-) Host Rat
- Catalog number:
- 'AM11136PU-S
- Product Quantity:
- 0.1 ml
- Category:
- -
- Supplier:
- ACR
- Gene target:
- G-CSF Clone 'SPM468 antibody Host Rat
Related genes to: G-CSF Clone 'SPM468 antibody Host Rat
- Gene:
- CSF3 NIH gene
- Name:
- colony stimulating factor 3
- Previous symbol:
- GCSF, G-CSF, C17orf33
- Synonyms:
- MGC45931
- Chromosome:
- 17q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
- Gene:
- CSF3R NIH gene
- Name:
- colony stimulating factor 3 receptor
- Previous symbol:
- CD114
- Synonyms:
- GCSFR
- Chromosome:
- 1p34.3
- Locus Type:
- gene with protein product
- Date approved:
- 1990-12-10
- Date modifiied:
- 2019-04-23
Related products to: G-CSF Clone 'SPM468 antibody Host Rat
Related articles to: G-CSF Clone 'SPM468 antibody Host Rat
- Fusobacterium nucleatum, a periodontal pathogen, has been increasingly implicated in pulmonary diseases including chronic obstructive pulmonary disease (COPD). This study demonstrates that F. nucleatum adheres to and invades pulmonary epithelial cells in a dose-dependent manner, primarily mediated by its adhesin FadA. We identify cadherin-11 (CDH11), which is upregulated in COPD lungs and in pulmonary epithelial cells treated with F. nucleatum or FadAc protein, as the key host receptor for FadA. This FadA-CDH11 interaction not only mediates bacterial adhesion and invasion, but also activates the MAPK13/JUN pathway, leading to significant upregulation of pro-inflammatory cytokines including CSF3, TNF-α, CCL20, and TGF-β. Genetic knockdown of CDH11 abolishes MAPK13/JUN activation and cytokine induction but does not affect FadA-mediated p53 suppression, indicating a separate pathway for this oncogenic event. Our findings establish the FadA-CDH11-MAPK13/JUN axis as a central mechanism driving F. nucleatum-exacerbated pulmonary inflammation and tissue damage, highlighting its potential as a therapeutic target for mitigating COPD progression. - Source: PubMed
Publication date: 2026/04/20
Liu KunXie XinyunLi YuchaoZhang ShuweiZang WenliLi QianPan Yaping - is a high-priority, emerging fungal pathogen frequently isolated from urine in healthcare settings. These isolates are often associated with indwelling urinary catheters, a primary risk factor for catheter-associated urinary tract infections (CAUTIs). Despite its clinical prevalence, the mechanisms of colonization and pathogenesis within the bladder remain poorly understood. In this study, we screened isolates from diverse clades using an biofilm model and murine models of uncomplicated UTI and CAUTI. While biofilm formation varied among isolates, the presence of a catheter significantly enhanced fungal burden in the bladder. Notably, one strain (B11103) caused rapid systemic dissemination and mortality. To address this, we evaluated a liquid-infused silicone (LIS) catheter coating, which has previously shown efficacy against other uropathogens. The LIS coating significantly reduced attachment and, crucially, mitigated fungal burden on both the catheter and bladder tissue across all tested strains. For the hypervirulent B11103 strain, LIS catheters also significantly reduced dissemination to the kidneys and bloodstream. Furthermore, cytokine analysis revealed that CAUTI upregulates IL-6, CSF3, and CXCL1; importantly, this damaging inflammatory response was also dampened by the LIS catheter. These findings demonstrate that catheterization potentiates pathogenicity and identify LIS catheters as a promising, antimicrobial-sparing strategy to prevent colonization, systemic spread, and inflammation during CAUTI.IMPORTANCEThis research addresses the critical public health challenge posed by the emergence of elucidating its pathogenesis in the urinary tract, the second-most common yet understudied reservoir. Here, we find that exhibits plasticity in its ability to form biofilms in urine and cause uncomplicated urinary tract infections (UTIs) and catheter-associated UTIs (CAUTIs). Importantly, we show that our liquid-infused silicone (LIS) catheters effectively disrupt this cycle by reducing fungal burden, preventing systemic spread, and dampening the damaging host inflammatory response. This work establishes the urinary tract as a critical niche for systemic entry and provides a validated strategy for infection prevention. Urinary catheters make dangerous, but this liquid-infused silicone coating is fighting back. - Source: PubMed
Publication date: 2026/04/15
La Bella Alyssa AnnAkegbe HopeHowell CaitlinSantiago-Tirado Felipe HFlores-Mireles Ana Lidia - Chronic substance use is a neuropsychiatric disorder marked by persistent craving, reward seeking, and progression to addiction. The midbrain governs hunger, reward, and pleasure; the DLPFC modulates craving, decision making, and tolerance; the NAc influences feeding, reward, stress, and drug self-administration; and the amygdala regulates emotion and memory. - Source: PubMed
Publication date: 2026/03/18
Veerappa AvinashGuda Chittibabu - Neuropathic pain is caused by lesions or disease affecting the somatosensory nervous system either in the periphery or centrally. Unresolvable inflammation is one of the main causes of the difficulty in managing prolonged pain. Although neuropathic pain is characterized by local inflammatory infiltration at the lesion site, whether neuropathic pain can induce systemic inflammation and the underlying mechanisms remain unknown. - Source: PubMed
Publication date: 2025/12/23
Chen ShangminZheng ZhikaiYing HuaYe FangLiao PengZhou JianTong SihanGao JunjieLiu DelinZhong ZhigangHuang Yi-Gang - Plasma proteomic profiling of 92 individuals with Post-Acute Sequelae of SARS-CoV-2 infection (PASC), assessed a mean of 34 months after acute infection, revealed a distinct inflammatory signature. Using proximity extension assay technology, 358 proteins were quantified, identifying 26 differentially expressed proteins (DEPs) in PASC: 23 upregulated and 3 downregulated. The most upregulated proteins were Oncostatin M (OSM) and IL-1 receptor antagonist (IL1RN). Additional increases were observed in IL-6, IL-12B, IL-2, CCL22, CSF3, CSF1, and HLA-DRA, as well as proteins involved in tissue remodeling and angiogenesis such as ANGPTL2 and TGFA. Random forest analysis confirmed IL1RN, OSM, ANGPTL2, HLA-DRA, and CLEC4A as strong discriminators between patients and controls. Gene set enrichment analysis demonstrated activation of multiple immune pathways, including Inflammatory Response, TNF-α/NF-κB signaling, IL-6/JAK/STAT3, IL-2/STAT5, and Allograft Rejection, indicating persistent activation of innate and adaptive immunity. STRING network analysis highlighted a tightly connected cytokine-driven inflammatory module. Plasma spike protein levels did not differ between patients and controls, suggesting that PASC-related inflammation may persist independently of ongoing viral replication. Overall, the findings indicate a consistent low-grade inflammatory state in PASC without evidence for distinct biological subtypes. - Source: PubMed
Publication date: 2026/02/23
Fineschi SerenaKlar JoakimSchuster JensBergquist JonasDahl Niklas