PubMed · 14258634
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I RANNIE. 1964-12-05. THE EPITHELIAL JUNCTION.. https://pubmed.ncbi.nlm.nih.gov/14258634/
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Both for tear films and along the airways within the lung, one has an extremely thin fluid layer overlying a biological substrate; in both cases surfactants either of natural origin, or artificially introduced, are important in driving fluid flows. There is evidence that slip can occur when hydrophilic liquids, similar to mucus or aqueous tear films, overlie hydrophobic epithelium. Utilizing results from recent experimental findings we examine the possible influence of slip upon tear film rupture, important in so-called dry eye, and upon surfactant-induced flows within the lung, used in surfactant replacement therapy.
The ability of the host to recognize pulmonary invasion by pathogenic organisms and establish an appropriate host response to infection requires innate immune defense mechanisms. Early bacterial clearance in the lung is mediated by alveolar macrophages (AM) and polymorphonuclear neutrophils. Additionally alveolar epithelial cells type II (AEC-II) may act as immunoregulatory cells. The toll-like receptors (TLR) are part of this innate immune defense, recognizing conserved patterns on microorganisms. Toll-like receptor 2 (TLR2) is crucial in detecting components of gram-positive bacteria and mycobacteria. Signals initiated by the interaction of TLR2 with bacterial components direct the subsequent inflammatory response. The detection of TLR2 mRNA in human lung tissue prompted us to localize the expression of mRNA and protein at the cellular level using a novel method for tissue fixation. We utilized HOPE-fixed lung specimen sections for targeting mRNA by in situ hybridization and protein by immunohistochemistry using the monoclonal antibody TL2.1. In normal lung areas the expression of TLR2 mRNA and protein was found to be located in cells resembling AEC-II and AM. Expression of mRNA was verified by RT-PCR and DNA sequencing. These results indicate a potential mechanism of increased immunosurveillance at the alveolar level controlling the localized infection.
Due to their low skin permeabilities, transdermal transport of hydrophilic solutes is poorly understood. In this study, we sought to determine the dependence of solute tortuosity on solute size and stratum corneum (SC) porosity. With porous pathway model, transdermal transport of hydrophilic solutes through the SC was modeled as diffusion through imperfections/defects that occur between/within the lipid lamellar organization of the SC. In order to seek an analytical solution, we assumed that the pores in the SC were cylindrical and organized in a cubical pattern. The proposed theoretical model describing the dependence of solute tortuosity on solute size and SC porosity is in agreement with prior experimentally derived tortuosity values.