[PubMed] [Google Scholar]Holmskov U, Lawson P, Teisner B, Tornoe I, Willis AC, Morgan C, Koch C, Reid KB. thus also giving them the name of Pathogen Recognition Receptor Proteins (Mayer et al., 2017) or PRRP’s. Collectins are a sub-type of c-type lectins which are characterized by a collagen-like domain with a short Cysteine-rich N-terminus (Drickamer et al., 1986). The structures of the majority of these proteins are similar, with a varying number of monomers binding to form multimeric structures. Each monomer is made up of four regions; a cysteine-rich domain at the N-terminus, a collagen-like domain, a coiled neck domain and a C-type lectin domain that is also called a carbohydrate recognition domain (CRD). Recognition of Icariin pathogens is mediated by the CRD in the presence of calcium (Petersen et al., 2001; Weis et al., 1992). To date, a host of collectins have been described including MBL, SP-A, SP-D, collectin liver 1 (CL-L1), collectin kidney 1 (CL-K1) and conglutinins (Mayer et al., 2017). These collectins recognize and neutralize pathogens by several different mechanisms including aggregation (Tenner et al., 1989), apoptosis (Liu et al., 2015), opsonization (Ferguson et al., 1999; Ghildyal et al., 1999; Hartshorn et al., 1996; Hickling et al., 1999; McIntosh et al., 1996; McNeely and Coonrod, 1994), activation of phagocytosis (Beharka et al., 2002; Ferguson et al., 1999; Nepomuceno Icariin et al., 1997; Tenner et al., 1989), inhibition of microbial growth, or modulation of Icariin the inflammatory response (Herbein and Wright, 2001; Liu et al., 2015; Saka et al., 2016; Salminen et al., 2008; Sato et Icariin al., 2003). Collectins may compete with factors such as LPS for binding to cell surface receptors (Chuang et al., 2011; Ohya et al., 2006; Saka et al., 2016; Vayrynen et al., 2002; Yamada et al., 2004). Some collectin-receptor interactions result in increased transcription of cytokines (Gardai et al., 2003) while others modulate the adaptive immune system by activation of T-lymphocytes (Gowdy et al., 2012; Pawaria and Binder, 2011), the modulation of antigen presentation by dendritic cells (Awasthi et al.; Steinberger et al., 2002; Yamada et al., 2004), or by mediation of IgE (Madan et Icariin al.), or histamine (Herias et al., 2007; Nayak et al., 2012) dependent allergic responses. Prior to the recognition of surfactant proteins as an independent entity, pulmonary mechanisms were defined in the context of the integrity of the alveolar surface and the substances which contributed to its function. It was in 1929 that Von Neergard, while describing the mechanics of the pulmonary system, suggested that a liquid film present INPP5K antibody on the alveolar surface might be important for the lowering of surface tension thereby modulating pulmonary mechanics (Von Neergaard, 1929). It was not until 1954, that Macklin elegantly described this mucoid substance (Macklin, 1954). He explained that the mucoid film has been credited with performing vital functions such as assisting in the removal of fine living and dead particulate matter, the maintenance of a constant favorable surface tension, the facilitation of gaseous exchange, the protection of the underlying tissue from desiccation and the suppression of invading microorganisms. This film, now known as surfactant, is produced by alveolar type II cells in the walls of the terminal respiratory alveolar structure in mature lungs. It is responsible for decreasing surface tension of the alveolar lining allowing the alveolus to remain distended to allow gas exchange at the alveolar epithelial surface. Surfactant is comprised of 80% lipids and 20% proteins, of which there are four surfactant proteins, namely, SP-A, SP-B, SP-C and SP-D (Hawgood and Clements, 1990). Alveolar type II cells, in the alveoli, produce and secrete all four of these surfactant proteins within lamellar bodies (Clements, 1957). Subsequently, SP-A and SP-D were also found in larger airways, secreted by sub-mucosal and Clara cells (Horowitz et al., 1991). Here, adsorption of the proteins is not necessary for airway function (Wong et al., 1996). SP-B and SP-C are involved in helping the spreading of surfactant across the alveolar lining and are also involved in surfactant metabolism and recycling. SP-A and SP-D, on the other hand are collectins with important roles.