Ticks jump in a warmer world: Global distribution shifts of main pathogenic ticks are associated with future climate change.

In recent decades, the threats of ticks and tick-borne diseases (TBDs) increased extensively with environmental change, urbanization, and rapidly changing interactions between human and animals. However, large-scale distribution of tick and TBD risks as well as their relationship with environmental change remain inadequately unclear. Here, we first proposed a "tick-pathogen-habitat-human" model to project the global potential distribution of main pathogenic ticks using a total of 70,714 occurrence records.

Isolation and whole genomic analysis of mesophilic bacterium in epithelial mesothelioma.

The relationship between bacteria and tumors has been the hot spot of clinical research in recent years. is an aerobic Gram-positive bacterium commonly found in soil. Recent studies have identified in patients with cutaneous and urinary tract infections.

Protective role of pyrroloquinoline quinone against gentamicin induced cochlear hair cell ototoxicity.

Gentamicin (GM) is one of the commonly used antibiotics in the aminoglycoside class but is ototoxic, which constantly impacts the quality of human life. Pyrroloquinoline quinone (PQQ) as a redox cofactor produced by bacteria was found in soil and foods that exert an antioxidant and redox modulator. It is well documented that the PQQ can alleviate inflammatory responses and cytotoxicity.

Tracing the future of epidemics: Coincident niche distribution of host animals and disease incidence revealed climate-correlated risk shifts of main zoonotic diseases in China.

Climate has critical roles in the origin, pathogenesis and transmission of infectious zoonotic diseases. However, large-scale epidemiologic trend and specific response pattern of zoonotic diseases under future climate scenarios are poorly understood. Here, we projected the distribution shifts of transmission risks of main zoonotic diseases under climate change in China.

Protective role for C3aR in experimental chronic pyelonephritis.

Emerging evidence suggest that C3aR plays important roles in homeostasis, host defense and disease. Although it is known that C3aR is protective in several models of acute bacterial infections, the role for C3aR in chronic infection is largely unknown. Here we show that C3aR is protective in experimental chronic pyelonephritis.

The C5a/C5aR1 Axis Contributes to the Pathogenesis of Acute Cystitis Through Enhancement of Adhesion and Colonization of Uropathogenic .

Our previous work using a murine model of pyelonephritis demonstrated that the C5a/C5aR1 axis plays a pathogenic role in acute kidney infection. In this study, we report that the C5a/C5aR1 axis also plays a pathogenic role in acute bladder infection. C5aR1-deficient mice had reduced bladder bacterial load and attenuated bladder tissue injury, which is associated with reduced expression of terminal α-mannosyl residues (Man) (a potential ligand for type 1 fimbriae of ) at the luminal surface of the bladder epithelium and reduced early bacterial colonization of the bladder.

Activation of the C3a anaphylatoxin receptor inhibits keratinocyte proliferation by regulating keratin 6, keratin 16, and keratin 17 in psoriasis.

Emerging evidence suggests that signaling through the C3a anaphylatoxin receptor (C3aR) protects against various inflammation-related diseases. However, the role of C3aR in psoriasis remains unknown. The purpose of this study was to investigate the possible protective role of C3aR in psoriasis and to explore the underlying molecular mechanisms.

Dopamine D3 receptor signaling alleviates mouse rheumatoid arthritis by promoting Toll-like receptor 4 degradation in mast cells.

Dopamine receptors are involved in several immunological diseases. We previously found that dopamine D3 receptor (D3R) on mast cells showed a high correlation with disease activity in patients with rheumatoid arthritis, but the mechanism remains largely elusive. In this study, a murine collagen-induced arthritis (CIA) model was employed in both DBA/1 mice and D3R knockout mice.

Circ_0003972 Promotes the Proliferation and Inflammation of Fibroblast-like Synovial Cells in Rheumatoid Arthritis through Regulation of the miR-654-5p/FZD4 Axis.

Background: Circular RNAs (circRNAs) have been shown to play an important role in rheumatoid arthritis (RA) progression. This study aims to explore the role and mechanism of circ_0003972 in RA progression.

Methods: Quantitative real-time PCR was used to determine gene expression.

Inhibition of fibroblast growth factor-inducible 14 attenuates experimental tubulointerstitial fibrosis and profibrotic factor expression of proximal tubular epithelial cells.

Background And Aim: As a proinflammatory cytokine, tumor necrosis factor-like weak inducer of apoptosis (TWEAK) participates in the progression of renal fibrosis by binding to its receptor, fibroblast growth factor-inducible 14 (Fn14). However, the effect of Fn14 inhibition on tubular epithelial cell-mediated tubulointerstitial fibrosis remains unclear. This study aimed to elucidate the role of TWEAK/Fn14 interaction in the development of experimental tubulointerstitial fibrosis as well as the protective effect of Fn14 knockdown on proximal tubular epithelial cells.

Antimicrobial Dose Selection under the Animal Rule.

The Food and Drug Administration's (FDA's) "Animal Rule" provides a unique regulatory pathway for drugs and biologics intended to treat serious or life-threatening conditions caused by exposure to lethal or permanently disabling chemical, biological, radiological, or nuclear agents when human efficacy studies are not ethical and field trials are not feasible. Human dose selection under the Animal Rule is based on integrating the totality of clinical pharmacology evidence collected in in vitro, animal, and human studies. This review discusses the necessary pharmacokinetic and pharmacodynamic information and methods for determining the effective human dose of antimicrobials under the Animal Rule and presents case studies illustrating the utility of a totality of evidence approach for different methods.

Approaches to Dose Finding in Neonates, Illustrating the Variability between Neonatal Drug Development Programs.

Drug dosing in neonates should be based on integrated knowledge concerning the disease to be treated, the physiological characteristics of the neonate, and the pharmacokinetics (PK) and pharmacodynamics (PD) of a given drug. It is critically important that all sources of information be leveraged to optimize dose selection for neonates. Sources may include data from adult studies, pediatric studies, non-clinical (juvenile) animal models, in vitro studies, and in silico models.

The C5a/C5aR2 axis promotes renal inflammation and tissue damage.

C5a is a potent inflammatory mediator that binds C5aR1 and C5aR2. Although pathogenic roles of the C5a/C5aR1 axis in inflammatory disorders are well documented, the roles for the C5a/C5aR2 axis in inflammatory disorders and underlying mechanisms remain unclear. Here, we show that the C5a/C5aR2 axis contributes to renal inflammation and tissue damage in a mouse model of acute pyelonephritis.

ALW peptide ameliorates lupus nephritis in MRL/lpr mice.

Background: Lupus nephritis (LN) is a common and serious complication of systemic lupus erythematosus. Anti-double-stranded (ds) DNA immunoglobulin G (IgG) plays a pivotal role in the pathogenesis of LN. Currently, there are various therapies for patients with LN; however, most of them are associated with considerable side effects.

TNF-α-elicited miR-29b potentiates resistance to apoptosis in peripheral blood monocytes from patients with rheumatoid arthritis.

CD14-positive monocytes from patients with rheumatoid arthritis (RA) are more resistant to apoptosis, which promotes their persistence at the inflammatory site and thereby contributes crucially to immunopathology. We sought to elucidate one mechanism underlying this unique pathogenesis: resistance to apoptosis and the potential involvement of miR-29b in this process. CD14-positive peripheral blood monocytes (PBMs) from RA patients were observed to be resistant to spontaneous apoptosis compared to PBMs from healthy volunteers.

UA promotes epithelial‑mesenchymal transition in peritoneal mesothelial cells.

Long‑term peritoneal dialysis is often limited or interrupted due to the development and progression of peritoneal fibrosis. Accumulating evidence suggests that epithelial‑mesenchymal transition (EMT) is a major component of peritoneal injury associated with peritoneal fibrosis in the end stage of renal disease; however, at present, the underlying mechanisms remain unclear. Thus, in the present study, uric acid (UA)‑induced EMT of peritoneal mesothelial cells was investigated by western‑blot and immunofluorescence staining.

The C3a/C3aR axis mediates anti-inflammatory activity and protects against uropathogenic E coli-induced kidney injury in mice.

Both the C3a/C3aR and C5a/C5aR1 axes are regarded as important pathways for inducing and regulating inflammatory responses. It is well documented that the C5a/C5aR1 axis is a potent inflammatory mediator in the pathogenesis of many clinic disorders. However, our understanding of the role of the C3a/C3aR axis in renal disorders remains limited.