HDRsEf1 Promotes Systemic Th1 Responses and Enhances Resistance to Infection.

The gut microbiota is known to regulate the immune system and thereby influence susceptibility to infection. In this study, we observed that the administration of HDRsEf1 (HDRsEf1) led to an improvement in the development of the immune system. This was evidenced by an increase in both the spleen index and the area of spleen white pulp.

Prevalence, drug resistance spectrum and virulence gene analysis of Campylobacter jejuni in broiler farms in central Shanxi, China.

This study collected 324 chicken cloacal swabs from 6 broiler farms in 4 different areas in Shanxi Province, China (i.e., Lvliang, Taiyuan, Jinzhong, and Yangquan), and analyzed the antimicrobial resistance and virulence-associated genes of the isolates to investigate the prevalence, drug resistance, and virulence gene data of Campylobacter jejuni in broilers.

The inflammatory cytokine IL-6 induces FRA1 deacetylation promoting colorectal cancer stem-like properties.

Colorectal cancer (CRC) has long been known for its tight association with chronic inflammation, thought to play a key role in tumor onset and malignant progression through the modulation of cancer stemness. However, the underlying molecular and cellular mechanisms are still largely elusive. Here we show that the IL-6/STAT3 inflammatory signaling axis induces the deacetylation of FRA1 at the Lys-116 residue located within its DNA-binding domain.

Colorectal cancer-derived small extracellular vesicles establish an inflammatory premetastatic niche in liver metastasis.

Liver metastases develop in more than half of the patients with colorectal cancer (CRC) and are associated with a poor prognosis. The factors influencing liver metastasis of CRC are poorly characterized, but this information is urgently needed. We have now discovered that small extracellular vesicles (sEVs; exosomes) derived from CRC can be specifically targeted to liver tissue and induce liver macrophage polarization toward an interleukin-6 (IL-6)-secreting proinflammatory phenotype.

ATR-CHK1-E2F3 signaling transactivates human ribonucleotide reductase small subunit M2 for DNA repair induced by the chemical carcinogen MNNG.

Background: N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), an alkylating agent and an environmental carcinogen, causes DNA lesions and even carcinomas. DNA damage responses induced by MNNG activate various DNA repair genes and related signaling pathways. The present study aimed to investigate the regulatory mechanisms of human RR small subunit M2 (hRRM2) in response to MNNG.

Aberrantly expressed Fra-1 by IL-6/STAT3 transactivation promotes colorectal cancer aggressiveness through epithelial-mesenchymal transition.

The pro-inflammatory cytokine interleukin-6 (IL-6) in tumor microenvironment has been suggested to promote development and progression of colorectal cancer (CRC). However, the underlying molecular mechanisms remain elusive. In this study, we demonstrate that fos-related antigen-1 (Fra-1) plays a critical role in IL-6 induced CRC aggressiveness and epithelial-mesenchymal transition (EMT).