Cytokine Gene Expression in Innately Susceptible BALB/c Mice and Relatively Resistant C57BL/6 Mice during Infection with VirulentBurkholderia pseudomallei

Abstract

Production of cytokines including gamma interferon (IFN-␥) and tumor necrosis factor alpha (TNF-␣

Toll-like Receptor 9 Regulates Tumor Necrosis Factor-α Expression by Different Mechanisms

“…Thus, our findings predict that pathological consequences of bacterial infections depend on the TNF-␣ allele expressed. It has indeed been shown that the two mouse strains we used respond in a different manner to bacterial infections (24,54). As a cytokine with a broad range of proinflammatory and immunostimulatory actions, TNF-␣ is thought to play a pivotal role in a number of human diseases including rheumatoid arthritis and periodontitis and a number of infectious and autoimmune diseases (55,56).…”

“…BALB/c and C57BL/6 express different TNF-␣ alleles and differ in the response of their innate immune system (17)(18)(19)(20)(21)(22)(23)(24). In light of the pivotal role of TNF-␣ in mediating the osteoclastogenic effect of CpG-ODN, we studied the induction of osteoclastogenesis and TNF-␣ expression in cells derived from mouse strains expressing different alleles of the cytokine.…”

Impaired IgG Production in Mice Deficient for Heat Shock Transcription Factor 1

“…PCR was performed as described using mouse gene-specific primers (18,19). The amplified DNA fragments were stained with ethidium bromide and photographed using Epi-Light UV FA1100 (Aisin Cosmos R&D Co., Japan).…”

Genetic Control of Survival and Weight Loss during Pneumonic Burkholderia pseudomallei (Bp) Infection

“…This results in a cellular response that fails to control the infection and contributes to tissue damage and multiple organ failure [56]. In contrast, B6 mice develop a chronic infection that is associated with a moderate but transient induction of pro-inflammatory cytokines, allowing the temporary sequestration of Bp within phagocytes and induction of an adaptive immune response [56,60]. The heighted level of resistance exhibited in B6 mice is thought to have a genetic basis.…”

“…The murine infection model has also been used to show both the importance of the host genetic background as well as host responses on the progression of a Bp infection [28]. BALB/c mice [57,58] and DBA/2J (D2) [55,59] mice are known to be extremely susceptible to the acute form of melioidosis, while C57BL/6 (B6) [28,55,56,58] mice exhibit a heightened level of resistance to the acute form of melioidosis, and tend to develop a chronic form of the disease. The acute melioidosis observed in BALB/c and D2 mice is characterized by significantly higher levels of pro-inflammatory cytokines, including a hyper-production of IFN-γ.…”