Permeability macrophage membrane

Robinson AV. 1982. Effect of in vitro exposure to hydrogen sulfide on rabbit alveolar macrophages cultured on gas-permeable membranes. Environ Res 27 491-500. 

The cell damage associated with inflammation acts on cell membranes to cause leukocytes to release lysosomal enzymes arachidonic acid is then liberated from precursor compounds, and various eicosanoids are synthesized. As discussed in Chapter 18, the cyclooxygenase (COX) pathway of arachidonate metabolism produces prostaglandins, which have a variety of effects on blood vessels, on nerve endings, and on cells involved in inflammation. The lipoxygenase pathway of arachidonate metabolism yields leukotrienes, which have a powerful chemotactic effect on eosinophils, neutrophils, and macrophages and promote bronchoconstriction and alterations in vascular permeability. 

Conventional liposomes and lipid complexes. Liposomes were used initially as a model system for cellular membranes to study the biochemistry of membrane proteins.85 Consequently, when liposomes were first tried as a drug delivery system, their bilayers were composed of un-derivatized naturally occurring lipids. Most of such conventional liposomes are taken up by the MPS phagocytes within a few hours of injection, mostly by liver Kupffer cells and spleen macrophages.9 Inside the endosomes and lysosomes of those cells, liposomes are degraded. If the liposomal drugs are membrane permeable, they then can diffuse from the endosomal compartments to the cytoplasm of the macrophage cells and slowly reenter the blood circulation. Because such a clearance... 

Inflammation is a common component associated with sepsis, meningitis, as well as respiratory tract, urinary tract, viral, and bacterial infections (Table 1). Bik is elevated during bacterial or viral infection. The presence of urinary Bik correlates well with standard urinalysis tests for urinary tract infections [20]. Endotoxins released from infectious pathogens induce inflammation and immune cell activation. Macrophages release interleukins and cytokines (IL-1, IL-6, IL-12, IL-15, IL-18, TNF-a) on exposure to lipo-polysaccharide (LPS) and lipoteichoic acid (LTA) endotoxins. These cytokines act as a chemotactic factors causing immune cell migration to the site of the infection followed by activation and release of proteases. Cytokines also induce increased vascular permeability in the endothelial. Bik suppresses further cytokine release by protease and intern additional migration and activation of immune cells. Additionally, a stabilization of the immune cell membrane prevents further release of proteases [4]. 

From a biological perspective, the finding of functioning hemichannels seems counterintuitive. There is an understandable bias that such large channels, if they were open, would rapidly kill cells by destruction of the selective permeability of the plasma membrane. However, the plasma membrane of macrophages and mast cells can become permeable to Lucifer Yellow [possibly through connexin channels (33)] for many minutes without lethal effect (115, 116). 

---