PgtE protease enables virulent to evade C3-mediated serum and neutrophil killing.

Non-typhoidal serovars, such as serovar Typhimurium (STm), are a leading cause of inflammatory diarrhea in otherwise healthy individuals. Among children, the elderly, and immunocompromised individuals, STm can spread to systemic sites and cause potentially lethal bacteremia. Phagocytic cells and the immune complement system are pivotal to preventing the dissemination of STm.

Inflammasome activation links enteric Typhimurium infection to a rapid, cytokine-dependent increase in intestinal mucin release.

The host restricts serovar Typhimurium infection of the gut via inflammasome-dependent sloughing of infected epithelial cells. Here we determined that concurrent caspase 1/11-dependent release of the goblet cell-derived mucin, Muc2, into the intestinal lumen also controls burdens in infected mice. The increased release of mucins from goblet cells in the cecum and nearby proximal colon, and the subsequent thickening of the protective mucus barrier layer in the distal colon, were all dependent on the cytokines interleukin (IL)-18 and IL-22, as deficiencies in either cytokine resulted in reduced mucin secretion.

Pathogenic diversification of the gut commensal via acquisition of a second type III secretion system.

is a Gram-negative bacterium found in various water and land environments and organisms, including insects and mammals. Some strains encode gene homologs of virulence factors found in pathogenic Enterobacterales members, such as serovar Typhimurium and . Whether these genes are pathogenic determinants in is not known.

Pathogenic diversification of the gut commensal via acquisition of a second type III secretion system.

is a Gram-negative bacterium found in a wide variety of water and land environments and organisms. It has been isolated as part of the gut microbiome of animals and insects, as well as from stool samples of patients with diarrhea. Specific strains encode gene homologs of virulence factors found in other pathogenic members of the same Enterobacterales order, such as serovar Typhimurium and Whether these genes are also pathogenic determinants in is not known.

Tocilizumab administration in cytokine release syndrome is associated with hypofibrinogenemia after chimeric antigen receptor T-cell therapy for hematologic malignancies.

Chimeric antigen receptor (CAR) T-cell therapy causes serious side effects including cytokine release syndrome (CRS). CRS-related coagulopathy is associated with hypofibrinogenemia that has up to now been considered the result of disseminated intravascular coagulation (DIC) and liver dysfunction. We investigated the incidence and risk factors for hypofibrinogenemia in 41 consecutive adult patients with hematologic malignancies (median age 69 years, range 38-83 years) receiving CAR T-cell therapy between January 2020 and May 2023 at the University Medical Center Regensburg.