- burn causes accumulation of cd11bf4/80 macrophages in periphery. expression of tlr2 and tlr4 increases in these macrophages early (3 days) after burn and decreases late (14 days). when tlr2 and 4 are ligated and macs are stimulated, there’s difference in cytokine expression profile, but it changes when either tlr2 or 4 are stimulated. (cairns 2008

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sarahhN9002 sarahhN9002

13-09-2022
Biology

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- burn causes accumulation of cd11bf4/80 macrophages in periphery. expression of tlr2 and tlr4 increases in these macrophages early (3 days) after burn and decreases late (14 days). when tlr2 and 4 are ligated and macs are stimulated, there’s difference in cytokine expression profile, but it changes when either tlr2 or 4 are stimulated. (cairns 2008

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tutorconsortium215 tutorconsortium215 · Answer 1 · 2022-09-15T11:57:30-04:00

After burn injury, complicated altered cytokine profiles are caused by toll-like receptor 2 and 4 ligation:

Background:

Toll-like receptor TLR2 and TLR4, expressed on innate immune cells, are important mediators of the immune response to pathogens.

In this study, we hypothesized that burn injury would lead to altered cytokine secretion profiles following her TLR2 or TLR4 ligation, associated with changes in her TLR expression in innate immune cells.

METHODS:

Female C56BL/6 mice were subjected to full-thickness burns or sham wounds of her 20%. At 3 or 14 days after her injury, whole spleen cells or purified splenic macrophages were cultured with her TLR2 ligand peptidoglycan or her TLR4 ligand lipopolysaccharide.

Supernatants were tested for TNF-α, MCP-1, IL-6, and IL-10. Cell death was assessed using flow cytometry. CD11b F4/80 congenital macrophages were sorted 14 days after burn injury and TLR2 and 4 expression was determined by quantitative reverse transcriptase polymerase chain reaction and flow cytometry.

RESULTS:

Burn injury results in a stable accumulation of CD11bF4/80 macrophages in the periphery. Purified macrophages early after burn injury upregulated TLR2 and 4, followed by a decrease in TLR2 and TLR4 expression late after burn injury.

Equivalent numbers of TLR2 and TLR4 ligated purified macrophages 3 days after thermal injury revealed no significant difference in cytokine secretion compared to sham. Stimulation 14 days after burn injury showed a significant decrease in tumor necrosis factor-α secretion by macrophages compared to sham mice.

In contrast, in the late post-burn period, interleukin-10 was significantly increased (mean approximately 1.8-fold) after either TLR2 or TLR4 stimulation. Interleukin-6 and monocyte chemoattractant protein-1 secretion were unchanged from sham levels.

In contrast, stimulation of whole splenocytes increased cytokines 3 and 14 days after burn injury. This effect may be caused by the accumulation of His TLR macrophages, which are resistant to TLR-induced cell death.

CONCLUSIONS:

Cytokine secretion profiles after TLR2 and TLR4 ligation after burn injury are altered in ways that do not clearly reflect anti- or pro-inflammatory states and are associated with intrinsic changes in populations. TLR2 and TLR4 ligation play complex and diverse roles in mediating the immune response to burn injury.

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