Expression of Toll-like receptor 4 in lungs of immune-suppressed rat with Acinetobacter baumannii infection

Abstract

Toll-like receptor 4 (TLR4) is involved in the regulation of host responses to Acinetobacter baumannii (A. baumannii). The aim of the present study was to examine the function of TLR4 in lung inflammation in immune-suppressed rats with A. baumannii infection. A total of 72 Sprague-Dawley male rats were randomly divided into the control, A. baumannii infection and immune-suppressed infection groups. The immune-suppressed infection group was treated with 100 mg/kg hydrocortisone by subcutaneous injection every other day for 2 weeks prior to A. baumannii infection. Lung tissue was obtained on the 3rd and 7th day after tracheal inoculation with A. baumannii. The expression of TLR4 in bronchial and alveolar epithelial cells, and alveolar macrophage was examined using immunohistochemistry. The levels of interleukin (IL)-6, tumor necrosis factor (TNF)-α in bronchoalveolar lavage fluid were detected using ELISA. The results showed that in the control group, the expression of TLR4 was upregulated in the bronchial and alveolar epithelial, and alveolar macrophages, and the levels of IL-6 and TNF-α were increased in the early phase of A. baumannii infection. On the 7th day, no significant difference in the levels of IL-6 and TNF-α was observed between the A. baumannii infection and control groups. Conversely, the expression of TLR4 was downregulated in the immune-suppressed group, and the levels of IL-6 and TNF-α were reduced on the 3rd day after infection. In the subsequent observation period, the expression of TLR4 was upregulated and the levels of IL-6 and TNF-α were increased. In conclusion, the results show a critical role of TLR4 in mediating effective immune response in the lung of rat with A. baumannii infection.

TAK-242 Attenuates Crush Injury Induced Acute Kidney Injury through Inhibiting TLR4/NF-κB Signaling Pathways in Rats

“…[22][23][24] Eventually, this produces a large number of inflammatory cytokines such as IL-6 and TNF-α. 25,26 These results suggested that the TLR4/NF-κB signaling pathway was involved in the process of crush injury induced AKI and promoted the release of inflammatory factors. When added TLR4 inhibitor in the crush groups, kidney function related indicators, such as creatinine, BUN, Mb, and potassium, were significantly improved, and the release of proinflammatory factors were significantly reduced.…”

Host Innate Immune Responses to Acinetobacter baumannii Infection

“…Studies using mouse and rat models have confirmed the important role of TLR4 in the host innate defense against respiratory and systemic A. baumannii infection (Knapp et al, 2006 ; Lin et al, 2012 ; Wang et al, 2016 ; Peng et al, 2018 ; Zhang et al, 2018 ). TLR4-/- mice were more susceptible to intranasal A. baumannii infection than wild-type mice (Knapp et al, 2006 ), with higher tissue bacterial burdens and more persistent infection.…”

Analysis of immune-related genes in idiopathic pulmonary fibrosis based on bioinformatics and experimental verification

“…Recent studies have shown that immunology plays an important role in the occurrence and development of IPF (18). For example, Toll-like receptor 4 (TLR4) is involved in the regeneration and renewal of type II alveolar epithelial cells, affecting the repair of lung injury and the formation of fibrosis (19,20). Macrophage infiltration and high levels of reactive oxygen species (ROS) have been shown to be the key characteristics of lung fibrosis (21).…”