Increased sensitivity of Corynebacterium parvum-treated mice to toxic effects of indomethacin and lipopolysaccharide

Abstract

Female BALB/c and C3H/HeJ mice develop increased sensitivity to the toxic effects of indomethacin after injection of nonviable Corynebacterium parvum. The increased sensitivity developed within 4 days of intraperitoneal injection of the organisms and started to resolve 14 days after injection. The development of increased sensitivity was dependent on the quantity of organisms injected and the concentration of indomethacin utilized. The effect was not observed when C. parvum-treated animals were injected with aspirin. C. parvum-treated BALB/c mice also developed increased sensitivity to E. coli lipopolysaccharide (LPS). Although increased sensitivity to LPS and indomethacin paralleled each other in BALB/c mice, the experiments with the LPS-resistant C3H/HeJ mice indicated that the two phenomena could be separated. The pyridine extract residue of C. parvum was as effective as C. parvum whole cells in inducing indomethacin and LPS sensitivity. Therefore, activation of the reticuloendothelial system is probably a critical element in the induction of sensitivity to these agents.

Qing-Re-Xiao-Zheng Formula Modulates Gut Microbiota and Inhibits Inflammation in Mice With Diabetic Kidney Disease

“…Desulfovbrionaceae and Desulfovibrio are LPS-producing bacteria ( 27 , 28 ), where LPS produced by Desulfovbrionaceae have potent inflammation-inducing capacities, usually 100- to 1,000-fold higher than LPS from Bacteroides spp ( 29 ), which are involved in gut permeability and chronic inflammation ( 30 ). As a potential human pathogen, Corynebacterium_1 could enhance an individual's susceptibility of LPS ( 31 ) and increase of the levels of inflammation ( 32 ). Peptostreptococcaceae , a bacterium that promotes inflammation, was more abundant in the DKD group ( 33 ).…”

Interleukin‐12 regulates natural killer cell‐dependent Propionibacterium acnes‐primed, lipopolysaccharide‐induced liver injury

“…[16][17][18][19][20][21] Liver injury and death in mice can be induced by the prior administration of the Grampositive bacteria Propionibacterium acnes (P. acnes), followed by a non-lethal dose of LPS. 22,23 In this model of hepatic injury, a dense infiltration of inflammatory cells and the production of pro-inflammatory cytokines are associated with liver necrosis and death. 22,24 The absence of significant liver injury in IFN-g-deficient mice versus that found in wild-type mice emphasizes the important role of IFN-g. [25][26][27][28][29][30] During the priming phase, IFN-g levels gradually increase during the mononuclear cell infiltration into the liver.…”

“…Early in the response to bacterial infections, macrophage‐derived IL‐12 induces IFN‐γ production by activated NK and T cells 8–11 and enhances NK cytotoxicity, 12–15 while later, the increased IL‐12‐induced IFN‐γ production promotes the proliferation of differentiated Th1 cells to bacterial antigens 16–21 . Liver injury and death in mice can be induced by the prior administration of the Gram‐positive bacteria Propionibacterium acnes ( P. acnes ), followed by a non‐lethal dose of LPS 22,23 . In this model of hepatic injury, a dense infiltration of inflammatory cellsand the production of pro‐inflammatory cytokines are associated with liver necrosis and death 22,24 .…”