PubMed · 16681313
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Carmel Duffin. 2006. Pathogen recognition by human lung epithelial cells.. https://pubmed.ncbi.nlm.nih.gov/16681313/
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OBJECTIVE: To examine the epithelial integrity of the inferior turbinate in patients with perennial allergic rhinitis (PAR) and perennial nonallergic (vasomotor) rhinitis (PNAR). DESIGN: Nonrandomized, controlled morphometric study. SETTING: University-affiliated hospital. PATIENTS: Fifty-eight inferior turbinate samples were processed for histological study. Nineteen were from patients with PAR, and 20 were from patients with PNAR. Samples from 19 healthy individuals who underwent rhinoplasty for cosmetic reasons served as control specimens. MAIN OUTCOME MEASURES: The length of the basement membrane (BM) covered with intact epithelium, covered with a single layer of basal cells, and devoid of epithelium was measured. RESULTS: Intact respiratory epithelium and areas of partial and complete epithelial denudation were encountered in control specimens and in samples from patients with PAR and PNAR. A significant difference was found between the 3 groups (P = .001). The proportion of the BM covered with undamaged epithelium was significantly greater in control specimens and in samples from patients with PNAR than in samples from patients with PAR; the difference between the former 2 groups was nonsignificant. Most of the epithelial damage in patients with PAR occurred between columnar and basal cells rather than between basal cells and the BM (P = .02). CONCLUSIONS: Epithelial shedding of the inferior turbinate is a genuine feature of PAR and is not an artifact of tissue sampling. The finding of greater epithelial exfoliation between basal cells and the more superficial columnar cells than between basal cells and the BM probably reflects different attachment qualities of these cells.
The innate immune system provides the first line of defence against infection. Through a limited number of germline-encoded receptors called pattern recognition receptors (PRRs), innate cells recognize and are activated by highly conserved structures expressed by large group of microorganisms called pathogen-associated molecular patterns (PAMPs). PRRs are involved either in recognition (scavenger receptors, C-type lectins) or in cell activation (Toll-like receptors or TLR, helicases and NOD molecules). TLRs play a pivotal role in cell activation in response to PAMPs. TLR are type I transmembrane proteins characterized by an intracellular Toll/IL 1 receptor homology domain that are expressed by innate immune cells (dendritic cells, macrophages, NK cells), cells of the adaptive immunity (T and B lymphocytes) and non immune cells (epithelial and endothelial cells, fibroblasts). In all the cell types analyzed, TLR agonists, alone or in combination with costimulatory molecules, induce cell activation. The crucial role played by TLR in immune cell activation has been detailed in dendritic cells. A TLR-dependent activation of dendritic cells is required to induce their maturation and migration to regional lymph nodes and to activate naïve T cells. The ability of different cell types to respond to TLR agonists is related to the pattern of expression of the TLRs and its regulation as well as their intracellular localization. Recent studies suggest that the nature of the endocytic and signaling receptors engaged by PAMPs may determine the nature of the immune response generated against the microbial molecules, highlighting the role of TLRs as molecular interfaces between innate and adaptive immunity. In this review are summarized the main biological properties of the TLR molecules.
The epithelial surface of the airways is the largest barrier-forming interface between the human body and the outside world. It is now well recognized that, at this strategic position, airway epithelial cells play an eminent role in host defense by recognizing and responding to microbial exposure. Conversely, inhaled microorganisms also respond to contact with epithelial cells. Our understanding of this cross talk is limited, requiring sophisticated experimental approaches to analyze these complex interactions. High-throughput technologies, such as DNA microarray analysis and serial analysis of gene expression (SAGE), have been developed to screen for gene expression levels at large scale within single experiments. Since their introduction, these hypothesis-generating technologies have been widely used in diverse areas such as oncology and brain research. Successful application of these genomics-based technologies has also revealed novel insights in host-pathogen interactions in both the host and pathogen. This review aims to provide an overview of the SAGE and microarray technology illustrated by their application in the analysis of host-pathogen interactions. In particular, the interactions between epithelial cells in the human lungs and clinically relevant microorganisms are the central focus of this review.